Printable list of all miscellaneous SAQs

College Answer

Rheumatoid arthritis is associated with a myriad of effects and complications. An ICU relevant list may include:

a) manifestations of the disease itself and its complications:

-     bone and joint destruction ( atlantoaxial subluxation)

-     vasculitis (renal impairment)

-     pulmonary fibrosis

-     neutropenia, anaemia, thrombocytopenia (eg Felty’s Syndrome)

b)   related to treatment

Steroids-  immunosuppression, skin changes, diabetes Methotrexate- immunosuppression, skin changes, diabetes NSAIDS- prone to renal failure, peptic ulcer disease etc Gold       penicillamine

From this it can be seen that the ways that RA influences ICU management may be manifold. The candidate was expected to briefly explain the consequences of these factors in the management of faecal peritonitis.

Discussion

The complications of rheumatoid arthritis, and the ways in which they influence critical care for these patients, is discussed in the answer to Question 30.1 from the first paper of 2008.

Copy-pasta again:

1. Difficult intubation, as caused by the abovementioned issues:
   1. Poor neck extension due to C-spine arthritis
   2. Risk of spinal cord injury due to atltantoaxial subluxation
   3. Poor mouth opening due to TMJ arthritis
   4. Poor vocal cord opening due to laryngeal arthritis or crico-arytenitis
   5. Poor respiratory reserve due to pulmonary fibrosis
   6. Difficulty assessing all of these issues in the context of an ICU intubation - you are not seeing this person in the pre-admission clinic; likely they are trying to die in some sort of advanced life support scenario.
2. Difficult mechanical ventilation:
   1. Oxygenation pproblems:
      1. Pulmonary fibrosis, diffusion defect
      2. Pulmonary hypertension
   2. Ventilation problems
      1. Pleural effusions
      2. Restrictive lung disease with poor complicance
   3. Weaning problems:
      1. Poor muscle strength due to steroid myopathy
      2. Delayed extubation if the intubation was difficult
3. Cardiac and vascular problems:
   1. Propensity to arrhythmias
   2. Increased risk of ischaemic heart disease
   3. Diastolic failure due to restrictive cardiomyopathy and pericardial disease make fluid resuscitation challenging
   4. Cardiac weirdopathy (eg. failure due to amyloid deposition needs to be considered in the differential diagnosis of an otherwise unexplained heart failure when the patient also has RA)
   5. Difficult vascular access (limb deformities)
   6. Poor mobility and deformity promotes the development of pressure areas
4. Neuropsychiatric problems:
   1. Steroid-induced psychosis - extubation may be interesting
   2. Psychological problems of chronic disease
   3. Increased analgesic requirements (chronic opiate/NSAID use)
5. Electrolyte and endocrine abnormalities associated less with RA than with its treatment:
   1. Chronic steroid use may promote hypoadrenalism
   2. Electrolyte derangement due to chronic steroid use
6. Renal problems:
   1. RA-associated (eg. glomerulonephritis, amyloidosis)
   2. Treatment-associated (eg. NSAID-induced damage)
   3. Does one commit to long term dialysis in this setting?
7. Gastrointestinal and nutritional problems:
   1. "Rheumatoid cachexia" due to cytokine-driven hypermetabolism promotes the need for more protein and calories (Roubenoff et al, 1994) - but it is unclear whether they benefit from "overfeeding", as they tend to become cachexic in spite of a theoretically adequate dietary intake.
   2. Gastic erosion/ulceration due to chronic steroid and NSAID use suggests that this group should get PPIs routinely
8. Haematological disturbances
   1. Anaemia of chronic disease: will you transfuse them?
   2. Thrombocytopenia (Felty's) - increased risk from neuraxial procedures and vascular access
9. Immune and infectious issues
   1. Increased risk of infection
   2. Increased propensity to be often seen in hospitals tends to result in increased risk of MRO colonisation
   3. Weird antiRA drugs may interact with antibiotics

References

College Answer

Mobile  chest  X-rays  are  essential  diagnostic  tools  in  ICU  but  are  subject  to  overuse  and misinterpretation.

Indications include: any ventilated patient with sudden respiratory or cardiovascular deterioration, after intubation, after insertion of NG tube, daily in critically ill ventilated patients and after insertion of CVC or ICC etc

The method: if possible the CXR should be erect with a consistent distance and energy used. Full inspiration should be held during exposure.

Precautions include: avoid in pregnant patients, cover genitalia in young patients particularly if long stay expected. Stay> 3 metres away from X-ray beam.

The useful information includes: position of lines etc., heart, mediastinal, soft tissue, bone and lung pathology (collapse, consolidation, effusion, oedema), trends in fluid status etc

Discussion

This question closely resembles Question 4 from the second paper of 2007, "Critically evaluate the clinical value of daily routine chest radiographs in the ICU."

References

College Answer

The essential characteristics of a transport ventilator for this role are :

•    easily portable (weighing <5 kg)

•    able to deliver air mix or 100% oxygen

•    able to be triggered by the patient when time cycled

•    consume only those gases equal to minute volume and therefore require minimum gas supply

•    compact size

•    able to ventilate a variety of patient sizes/ages

•    have airway pressure and apnoea alarms built in

•    able to use variable PEEP

Ideal range of features may include:

•    Capability for a variety of modes eg SIMV, PSV

•    Variable FiO2

Discussion

This question is a direct rip-off of Table 4.2 (page 32) from Oh's Manual, "Features of an Ideal Transport Ventilator".

The features listed in this table include the following:

• Small, light, robust and cheap
• Independent of an external power wource
• Easy to use and clean
• Economical with gas consumption
• Suitable for patients of all sizes, from neonates to huge adults
• Totally variable FiO₂
• Able to deliver a variety of modes of ventilation
• Able to ventilate with variable I:E ratios
• Integrated monitoring and alarm functions
• Alarms should be visual and auditory
• Altitude compensated ventilation

References

Oh's Intensive Care manual:

• Chapter 4 (pp.27)    Transport  of  critically  ill  patients   by Evan  R  Everest  and  Matthew  R  Hoope

College Answer

Initial management involved complete evaluation and staging, close monitoring, and providing adequate pain relief.   Further treatment involves correcting any precipitating factors, review preventative measures, correct nutritional status (deficiencies diagnosed and corrected), manage tissue pressure (eg. specialised beds) remove necrotic tissue, manage wound infections and maintain a moist environment.

Preventative techniques require identification of patients at risk, daily skin inspections, patient positioning (two hour turning, pressure reducing mattresses, special beds), encouraging mobility (physical therapy, reduce sedatives), and provision of adequate nutrition.

Discussion

LITFl have a nice section on pressure areas. A structured approach would resemble the following:

Risk factors for pressure ulcers in ICU

A good article from 2000 has an exhaustingly long table (Table 1).

Highlights from this article include the following:

• Prolonged immobility
• Use of neuromuscular junction blockers
• Age over 60
• Severe illness (APACHE II score over 13)
• Hemodynamic instability preventing pressure area care
• Diabetes
• Incontinence
• Low albumin
• Poor nutrition
• Oedema
• Peripheral vascular disease
• Steroid use

Prevention of pressure ulcers in ICU

• Risk assessment and monitoring
• Mobility (may be unreasonable in this context)
• Minimise sedation and restraints to allow for self-repositioning (may not be relevan in this context)
• Management of incontinence
• 2 hourly repositioning
• Air mattress or specialised foam (evidence is not strong)
• Adequate skin care

Management of pressure ulcers in the ICU

• Engagement of a multidisciplinary wound care team
• Debridement
• Antibacterial (silver sulfadiazine) dressings
• Frequent dressing changes
• Exudate-absorbing dressings
• Promote wound healing:
  • Adequate nutritional supplementation, particularly of protein (2g/kg/day)
  • Control of diabetes
  • Avoidance of corticosteroids
  • Optimisation of tissue perfusion
  • Avoidance of oedema

References

Keller, Paul B., et al. "Pressure ulcers in intensive care patients: a review of risks and prevention." Intensive care medicine 28.10 (2002): 1379-1388.

Cullum, N., et al. "Beds, mattresses and cushions for pressure sore prevention and treatment." The Cochrane Library (2000).

REULER, JAMES B., and THOMAS G. COONEY. "The pressure sore: pathophysiology and principles of management." Annals of Internal Medicine94.5 (1981): 661-666.

Health Quality Ontario. "Pressure Ulcer Prevention: An Evidence-Based Analysis." Ontario health technology assessment series 9.2 (2009): 1.

Stratton, Rebecca J., et al. "Enteral nutritional support in prevention and treatment of pressure ulcers: a systematic review and meta-analysis." Ageing research reviews 4.3 (2005): 422-450.

Henzel, M. Kristi, et al. "Pressure ulcer management and research priorities for patients with spinal cord injury: consensus opinion from SCI QUERI Expert Panel on Pressure Ulcer Research Implementation." J Rehabil Res Dev 48.3 (2011): xi-xxxii.

Theaker, C., et al. "Risk factors for pressure sores in the critically ill."Anaesthesia 55.3 (2000): 221-224.

College Answer

Many different strategies are employed and should be considered.  Reviews and recommendations are widely published (eg. Geerts, WH, Heit, JA, Clagett, GP, et al.   Prevention of venous thromboembolism. Chest 2001; 119:132S). Good placebo controlled RCTs are rare.

Simple techniques such as passive mobilisation, and early active mobilisation are encouraged but not well studied.  The use of elastic compression stockings (knee-length or whole leg) is simple, widespread and effective for low risk patients.  The addition of intermittent pneumatic compression devices has been recommended (limited evidence) where higher risk exists but other pharmacology is deemed contraindicated.  Most studies have assessed the use of low dose unfractionated heparin or low molecular weight heparins (though few studies have used placebo control).  LMW heparins (when compared with unfractionated heparin) seem to provide similar or better prophylaxis, with less thrombocytopaenia, though with a small increase in the incidence of bleeding.  Other agents including pentasaccharides or hirudin are showing promise.  Older agents such as dextran and warfarin are used less frequently.

Other controversies include cost-benefit, and side-effect profiles etc.

Discussion

A systematic approach to this answer would resemble the following:

Rationale:

• DVT develops in a large proportion of ICU patients in the absence of DVT prophylaxis:
  • 30% of general medical/surgical ICU patients
  • 50-65% of trauma patients
  • 20%-50% of neurosurgical patients
  • 80% of spinal cord injury patients
• VTE is a significant cause of ICU mortality and morbidity
• Even small emboli may be disastrous

Therapeutic options

• Unfractionated heparin
• Low molecular weight heparin
• Compression stockings
• Sequential pneumatic compression devices
• Early mobilisation

Advantages:

• Cost-effective prevention of mortality and morbidity

Disadvantages:

• Risk of bleeding with chemical methods
• Risk of DVT dislodgement with pneumatic compression
• Risk of falls with ealry mobilisation
• Risk of limb ischaemia with compression stockings
• Contraindicated in lower limb surgery or trauma

Evidence:

• The recommendation for early mobilisation is based on the knoweldge that immobility is associated with DVT, rather than on any sort of prospective trial evidence.
• Heparin of any sort is protective against DVT (16 studies with a combined n=34,369)
• No difference between LMWH and UHF (PROTECT trial)
• Intermittent compression stockings are better than nothing according to a recent prospective cohort study.
• Compression stockings in the ICU are purely decorative according to the same study, but in the general hospital population they are better than nothing, and have a cumulative benefit when used together with other methods of DVT prophylaxis.
• Authors trend towards the suggestion that a combination of chemical and mechanical methods is the best practice

The PROTECT trial (2011) is the most recent large entry into the DVT prophylaxis arena. It was negative- there was no difference between LMWH and UFH. However, a significant reduction in the incidence of PE was found with LMWH, which has led some authors to recommend it as the first choice in renally normal patients.

References

LIFL have an excellent page on VTE prophylaxis in the ICU.

Cook, Deborah, et al. "Dalteparin versus unfractionated heparin in critically ill patients." The New England journal of medicine 364.14 (2011): 1305-1314.

Attia, John, et al. "Deep vein thrombosis and its prevention in critically ill adults." Archives of Internal Medicine 161.10 (2001): 1268-1279.

Arabi, Yaseen M., et al. "Use of Intermittent Pneumatic Compression and Not Graduated Compression Stockings Is Associated With Lower Incident VTE in Critically Ill Patients Mechanical Prophylaxis in Critically Ill Patients A Multiple Propensity Scores Adjusted Analysis." CHEST Journal 144.1 (2013): 152-159.

Sachdeva, Ashwin, et al. "Elastic compression stockings for prevention of deep vein thrombosis." Cochrane Database Syst Rev 7.7 (2010).

Alikhan, Raza, Rachel Bedenis, and Alexander T. Cohen. "Heparin for the prevention of venous thromboembolism in acutely ill medical patients (excluding stroke and myocardial infarction)." status and date: New search for studies and content updated (no change to conclusions), published in 5 (2014). Cochrane Database of Systematic Reviews 2014, Issue 5.

College Answer

Few studies have addressed the potential benefits of clinical examination in the critically ill.  Those that have addressed estimation of filling pressures have been disappointing.  In general benefits of clinical examination are only supported by lower levels of evidence (including extrapolation from other patient populations).

In the critically ill, as history may be difficult to obtain, especially in an emergency, clinical signs alone are used to guide treatment and investigation until more definitive information is available. Candidates should discuss potential risks & benefits (eg. early detection guiding treatment vs lack of sensitivity [missing disease states] and sensitivity [wrongly excluding differential diagnoses].

Types of information that are available and may influence management (either in an emergency or otherwise) include: assessment of airway and breathing (eg. position of ETT cuff, chest movement, breath sounds), circulation (eg. presence of pulses: peripheral/central and estimate of peripheral perfusion); neurological assessment (AVPU/GCS/pupils, localising signs, tone & reflexes, sensation);  presence  of  skin  lesions  (rash:  purpura,  erythematous,  papular;  spider  naevi  etc); localised tenderness (eg. limb, abdominal quadrant etc); presence of abnormal masses (eg. lymph nodes,  hepatosplenomegaly);  fundoscopic  assessment  (eg.  subhyaloid  haemorrhages, papilloedema); assessment of invasive devices/dressings/drains etc.

Discussion

Rationale:

• History and physical examination is the mainstay of diagnosis in non-ICU environments
• ICU patients are frequently unable to offer a history
• Physical examination may be able to reveal new pathology, which would otherwise have not been suspected from routine bloods and radiography.
• Clinical features are more reliable than other methods in the diagnosis of certain conditions (eg. delirium, weakness, etc)

Advantages:

• Cheap
• Non-invasive (mostly)
• Sequential
• May detect deterioration early
• Better than imaging for neurological assessment
• Assesses function as well as structure
• Many ICU devices enhance physical examination technique (eg. CVP waveform supercedes the examination of the JVP)

Disadvantages:

• Poor sensitivity and specificity
• New pathology may be missed
• Interpreter-dependent
• Poor reproduceability of findings
• Many barriers to traditional techniques in the ICU (eg. the patient is uncooperative, dressings and lines obscure physical signs)

Evidence:

• Little evidence in support of this widespread practice
• Benefits of clinical examination are extrapolated from outpatient population.
• A survey of ICU physicians from California has revealed that 59% think physical examination has limited utility, and 94% uncluded non-classical components (such as assessment of arterial and ventilator waveforms). Everybody was in agreement that percussion was the least useful physical sign.

References

Rudiger, A. "[The clinical examination of the critically ill patient in the intensive care unit]." Therapeutische Umschau. Revue therapeutique 63.7 (2006): 479-484.

Sackett, David L. "A primer on the precision and accuracy of the clinical examination." Jama 267.19 (1992): 2638-2644.

Dobb, G. J., and L. J. Coombs. "Clinical examination of patients in the intensive care unit." British journal of hospital medicine 38.2 (1987): 102-4.

Hillman, K., G. Bishop, and A. Flabouris. "Patient examination in the intensive care unit." Intensive Care Medicine. Springer New York, 2002. 942-950.

Guillamet, R. Vazquez, et al. "Physicians Perceptions Of The Utility Of Physical Exam In The Intensive Care Unit. A Qualitative Study." Am J Respir Crit Care Med 185 (2012): A1661.

College Answer

CREST syndrome refers to the predominantly cutaneous rheumatological condition with Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly and Telangiectasia. Associated conditions include scleroderma (with additional arthralgias, myalgias, contractures, pulmonary fibrosis and pulmonary hypertension, renal impairment etc.).   Patients with CREST syndrome therefore may have many manifestation that may complicate ICU management.  Some of the many resultant potential problems include difficult intubation (limited mouth opening), risk of aspiration (and oesophageal perforation with TOE), malabsorption and nutritional deficiencies, limited respiratory reserve, risk of digital ischaemia with radial arterial lines and vasoconstrictors, skin breakdown/pressure area, and propensity to renal failure.

Discussion

CREST stands for:

• Calcinosis
• Raynauds
• oEsophagitis
• Sclerodactily
• Telangiectasia

It is a member of the scleroderma family of disorders. In fact, its "scleroderma light" - the limited form of systemic sclerosis.

The factors which influence the ICU management of scleroderma therefore also apply to CREST. These are discussed in greater detail in the answer to Question 28 from the first paper of 2012. That answer is reproduced below:

1.  Difficult intubation:
   1. Limited neck extension
   2. Limited mouth opening
2.   Respiratory involvement:
   1. Pulmonary fibrosis
   2. Restrictive lung disease
   3. Pulmonary hypertension
   4. SpO₂ monitoring may be frustrated by poor end-digital perfusion
   5. The rapidly fatal "scleroderma-pulmonary-renal syndrome (SPRS)" may develop, which manifests as a fulminant course of acute normotensive renal failure associated with diffuse alveolar hemorrhage.
3. Cardiovascular involvement of the disease process:
   1. Cardiac problems:
      1. Arrhythmias,
      2. Myocardial fibrosis (thus, restrictive diastolic failure)
      3. Pericardial stricture (also restricts diastolic filling)
   2. Vascular problems
      1. Difficult vascular access: the skin, being very thick, makes it difficult to palpate vessels (veins and arteries both)
      2. Poor distal perfusion of the extremities, leading to gangrene- as one might expect this is not improved by arterial cannulation.
      3. Poor skin perfusion promotes pressure areas
4. Neurological sequelae: 
   1. Corticosteroid-associated psychosis
   2. Cerebral vasculitis
5. Electrolyte disturbances
   1. Hyponatremia and fluid retention due to corticosteroid therapy
   2. Hyperkalemia due to renal failure
6. Renal involvement
   1. Renal failure, renal artery stenosis
   2. Scleroderma "renal crisis"
7. Gastrointestinal and nutritional issues
   1. Oesophagitis
   2. Poor gut motility
   3. Decreased feed tolerance
   4. Risk of aspiration.
   5. Risk of oesophageal perforation
   6. Telangiectasia is present also on mucosal surfaces; there is an increased risk of bleeding from upper GI sites
8. Haematological problems:
   1. Anaemia of chronic disease is coupled with the poor EPO synthesis from damaged kidneys.
   2. Bone marrow function may be suppressed in other ways, particularly if serious immunosuppresants are in use (eg. cyclophosphamide)
9.     Immunosuppressive therapy
   1. Increased infection risk

References

Farber, Harrison W., Robert W. Simms, and Robert Lafyatis. "Analytic Review: Care of Patients With Scleroderma in the Intensive Care Setting." Journal of intensive care medicine 25.5 (2010): 247-258.

Legerton 3rd, C. W., Edwin A. Smith, and Richard M. Silver. "Systemic sclerosis (scleroderma). Clinical management of its major complications."Rheumatic diseases clinics of North America 21.1 (1995): 203-216.

College Answer

Two inter-collegiate documents have been published (PS39 and IC-10) and cover the principles of management in detail.  Intra-hospital transport requires justification of transport (review of risks vs benefits), availability of appropriate and functional equipment (monitoring and emergency intervention), adequately skilled staff, appropriate pre-departure procedures (including checking of equipment and drugs, and accompanying patient records/investigations), planning of appropriate timing  and  route,  confirmation  of  appropriate  clinical  status  before  transport,  appropriate monitoring during transport, assessment of monitoring and equipment at destination, appropriate handover if another team assumes responsibility for care, appropriate documentation of clinical status during transport and some process to  facilitate quality assurance. Inter-hospital or pre- hospital transport also includes consideration of mode of transport (distance vs efficiency vs risks of road/fixed  wing/helicopter), and  potential  preventative procedures  before  transport  (e.g.  chest tubes).  For all transports, some forms of monitoring are considered mandatory (i.e. pulse oximetry, capnography [if mechanically ventilated], ECG, and blood pressure).

Discussion

This question is identical to Question 7 from the second paper of 2005.

References

College Answer

SLE is a chronic inflammatory disease, presumably auto-immune, which occurs predominantly in women, and can affect almost all organ systems. These can masquerade as many different conditions, and can make workup very complex. Clinical features (and examples of ways they would influence management) include:

•    Fatigue (common and debilitating)- care with differential diagnosis

•    Fever (episodic and related to activity of disease)- need to exclude sepsis, potential for un-necessary antibiotics

•    Arthritis (painful, migratory and asymmetrical; rarely deforming)- care with positioning, may need analgesia

•    Skin changes (butterfly rash, and hair loss)- care with handling

•    Raynaud’s phenomenon- caution with vasoconstrictors, pulse oximeters, arterial lines

•    Renal dysfunction (usually glomerulonephritis)- avoid nephrotoxins, adjust drug doses

•    Pleurisy and pleural effusions- need to diagnose, exclude other conditions

•    Pericarditis and Libman-Sacks (verrucous) endocarditis- may require TOE or surgery

•    Increased incidence of coronary artery disease- need to be aware of problem in otherwise young females without risk factors!

•    Delerium, psychosis and seizures- complex management and diagnostic problem

•    Thrombosis in association with anti-phospholipid antibodies- need to diagnose, and may need treatment for pro-coagulant state

•    Abnormal haematology (leukopenia, anaemia, thrombocytopenia)- may need further investigation

•    Lymphadenopathy and splenomegaly- may make suspicious of alternative disease process; may ned further investigation

•    Auto-immune disease and immunosuppressive therapy (eg. corticosteroids, cyclophosphamide)- at particular risk of infections in immunosuppressed. Early and aggressive workup and initial treatment may be required. Aware of potential for adrenal suppression.

Discussion

This question would benefit from a structured tabulated answer.

References

Good, J. T., et al. "Lupus pleuritis. Clinical features and pleural fluid characteristics with special reference to pleural fluid antinuclear antibodies."CHEST Journal 84.6 (1983): 714-718.

HELLMANN, DAVID B., MICHELLE PETRI, and Q. U. I. N. N. WHITING-O'KEEFE. "Fatal infections in systemic lupus erythematosus: the role of opportunistic organisms." Medicine 66.5 (1987): 341-348.

Urbanus, Rolf T., Ronald HMW Derksen, and Philip G. de Groot. "Current insight into diagnostics and pathophysiology of the antiphospolipid syndrome."Blood reviews 22.2 (2008): 93-105.

Kokori, Styliani IG, et al. "Autoimmune hemolytic anemia in patients with systemic lupus erythematosus." The American journal of medicine 108.3 (2000): 198-204.

Giannouli, Stavroula, et al. "Anaemia in systemic lupus erythematosus: from pathophysiology to clinical assessment." Annals of the rheumatic diseases65.2 (2006): 144-148.

Van Steenbergen, Werner, et al. "‘Lupus’ anticoagulant and thrombosis of the hepatic veins (Budd-Chiari syndrome): Report of three patients and review of the literature." Journal of hepatology 3.1 (1986): 87-94.

Sultan, S. M., Y. Ioannou, and D. A. Isenberg. "A review of gastrointestinal manifestations of systemic lupus erythematosus." Rheumatology 38.10 (1999): 917-932.

Cameron, J. Stewart. "Lupus nephritis." Journal of the American Society of Nephrology 10.2 (1999): 413-424.

Bruce, Ian N., et al. "Risk factors for coronary heart disease in women with systemic lupus erythematosus: the Toronto Risk Factor Study." Arthritis & Rheumatism 48.11 (2003): 3159-3167.

Sanders, E. A. C. M., and L. A. H. Hogenhuis. "Cerebral vasculitis as presenting symptom of systemic lupus erythematosus." Acta neurologica scandinavica 74.1 (1986): 75-77.

Jacobson, Edwin J., and Michael J. Reza. "Constrictive pericarditis in systemic lupus erythematosus. Demonstration of immunoglobulins in the pericardium."Arthritis & Rheumatism 21.8 (1978): 972-974.

Busteed, S., et al. "Myocarditis as a prognostic indicator in systemic lupus erythematosus." Postgraduate medical journal 80.944 (2004): 366-367.

Turner-Warwick, Margaret, and Deborah Doniach. "Auto-antibody studies in interstitial pulmonary fibrosis." British medical journal 1.5439 (1965): 886.

Asherson, R. A., et al. "Pulmonary hypertension in systemic lupus erythematosus." British medical journal (Clinical research ed.) 287.6398 (1983): 1024.

Nanke, Y. U. K. I., et al. "Cricoarytenoid arthritis with rheumatoid arthritis and systemic lupus erythematosus." The Journal of rheumatology 28.3 (2001): 624-626.

Martin, L., et al. "Upper airway disease in systemic lupus erythematosus: a report of 4 cases and a review of the literature." The Journal of rheumatology19.8 (1992): 1186-1190.

Cervera, Ricard, et al. "Morbidity and mortality in systemic lupus erythematosus during a 10-year period: a comparison of early and late manifestations in a cohort of 1,000 patients." Medicine 82.5 (2003): 299-308.

College Answer

TEN is condition involving rapid progression of erythems and extensive (usually > 30% epidermis involved) epidermal necrolysis. It overlaps with the Stevens-Johnson syndrome, and has a high mortality rate (up to 44%!). Early dermatological consultation is important. Diagnostic features include:

•    Skin eruption that begins 1-3 weeks after starting a suspicious drug

•    A prodrome of fever and flu-like symptoms, 1-3 days before eruption

Poorly defined macules with purpuric centres that coalesce to form blisters, and then epidermal detachment (involving > 30% epidermis)

•    Symmetrical, primarily over face and upper trunk

•    Burning or painful lesions (with complications similar to extensive thermal burns)

•    Mucosal involvement in 90% (eg. conjunctiva, mouth, oesophagus, genital)

•    Pulmonary complications can occur (eg. excessive-secretions, sloughing of bronchial epithelium, BOOP)

Most cases are drug induced, few are idiosyncratic.  The commenest drugs to be implicated are:  sulphonamides  antibiotics,  aminopenicillins,  quinolones,  cephalosporins, carbemazepine, phenobarbital, phenytoin, valproic acid, NSAIDs, allopurinol and corticosteroids! TEN is more common in patients with SLE and HIV.

Discussion

Stevens-Johnson Syndrome and TEN are considered diseases of the same spectrum. SJS is the less severe classification of the same disease: only ~ 10% of the skin surface is sloughed. TEN, on the other hand, is a condition of over 30% slough. In the 10-30% patients, the two conditions overlap. This condition had come up again thirteen years later, in Question 28 from the second paper of 2018 which asked for a lot more detail about TEN, and which was actually done much better (pass rate was 58.2%).

Thus, the diagnostic features:

• History of exposure to a new drug
• 1-3 weeks of waiting
• Fever and flu-like symptoms for 1-3 days before skin eruption
• Skin eruption: poorly defined macules with purpuric centres
• Then, blisters and epidermal detachment
• Symmetrical, primarily over face and upper trunk
• Complications similar to burns
• Mucosal involvement in 90%
• BOOP and respiratory mucosal sloughing can also occur

Drugs which are known to cause TEN:

• phenytoin
• NSAIDs
• Penicillins
• Quinolones
• Carbamazepine
• Valproate
• Allopurinol
• Fluconazole
• Sulfonamides
• Barbiturates

Non-drug causes of TEN:

• Mycoplasma pneumoniae (next most common cause)
• HIV
• HSV
• Influenza virus
• Coxsackie
• Mumps
• Malignancy (though this is usually listed as a risk factor or association)

References

Gerull, Roland, Mathias Nelle, and Thomas Schaible. "Toxic epidermal necrolysis and Stevens-Johnson syndrome: A review*." Critical care medicine39.6 (2011): 1521-1532.

Wiler, Jennifer L. "Diagnosis: Toxic Epidermal Necrolysis." Emergency Medicine News 29.9 (2007): 20-21.

Roujeau, Jean-Claude, et al. "Toxic epidermal necrolysis (Lyell syndrome)."Journal of the American Academy of Dermatology 23.6 (1990): 1039-1058.

Shiga, Sarah, and Rob Cartotto. "What are the fluid requirements in toxic epidermal necrolysis?." Journal of Burn Care & Research 31.1 (2010): 100-104.

Fromowitz, Jeffrey S., Francisco A. Ramos‐Caro, and Franklin P. Flowers. "Practical guidelines for the management of toxic epidermal necrolysis and Stevens–Johnson syndrome." International journal of dermatology 46.10 (2007): 1092-1094.

College Answer

Many candidates failed to mention guidelines, monitoring, handover or documentation.
Two inter-collegiate documents have been published (PS39 and IC-10) and cover the principles of management in detail. Intra-hospital transport requires justification of transport (review of risks vs benefits), availability of appropriate and functional equipment (monitoring and emergency intervention), adequately skilled staff, appropriate pre-departure procedures (including checking of equipment and drugs, and accompanying patient records/investigations), planning of appropriate timing and route, confirmation of appropriate clinical status before transport, appropriate monitoring during transport, assessment of monitoring and equipment at destination, appropriate handover if another team assumes responsibility for care, appropriate documentation of clinical status during transport and some process to facilitate quality assurance. Inter-hospital or pre- hospital transport also includes consideration of mode of transport (distance vs efficiency vs risks of road/fixed wing/helicopter), and potential preventative procedures before transport (e.g. chest tubes). For all transports, some forms of monitoring are considered mandatory (i.e. pulse oximetry, capnography [if mechanically ventilated], ECG, and blood pressure).

Discussion

This question closely resembles Question 7 from the second paper of 2010 and Question 9 from the second paper of 2012., though they deal primarily with aeromedical and interhospital transfer.

In brief:

Justification for transfer

• All should agree that the benefit outweighs the risk

Interhospital transfer vehicle

• Determined by nature of illness and urgency or retrieval
• Need to be mindful of the effects of transport on the illness (eg. the effect of low cabin pressure on gas-filled obstructed bowel loops)
• Number of staff and volume of equipment
• Road conditions, weather conditions

Equipment

• Airway equipment
• Suction
• Ventilator
• Oxygen supply (in excess)
• Defibrillator
• Thermal insulation
• Monitoring equipment
• All drugs checked and labelled

Monitoring

• Pulse oximeter
• Capnometer
• ECG
• NIBP or arterial line
• Airway equipment must have disconnection alarms

Patient preparation

• Ideal patient is intubated, ventilated and paralysed
• The patient should ideally be stabilised on a transport ventilator before departure
• Vascular access should be secure; you should not be doing any elective procedures during transfer
• One last pre-departure assessment

Communication:

• Confirmation that the destination is aware of transfer, and is ready
• Documentation travels with the patient

References

ANZCA "Guidelines for Transport of Critically Ill Patients

CICM "Minimum Standards for Transport of Critically Ill Patients" (IC-10, 2010)

College Answer

The potential roles of ultrasound in critically ill patients are diverse and are increasing in number.

They include:

Cardiac echo – transthoracic/transoesophageal looking at structure, function, relationships between the two and pericardial effusions, and doppler cardiac output monitoring.

Vascular –thoracic and abdominal aorta (dissection, aneurysm etc). Other vascular roles include any accessible artery (eg radial, brachial, femoral, carotid etc), grafts for flow assessment, stenosis, patency. Also larger veins for thrombosis/patency, and vessel identification for line insertion

Cranial – monitor cerebral blood flow, hyperaemia, ischaemia, detection of vasospasm, fat and other emboli, stroke related artery reperfusion following thrombolysis.

Renal perfusion – following AAA repair, renal transplant and acute tubular necrosis.

Free fluid – peritoneal and pleural – allows diagnosis, quantitative assessment as well as marking for drainage.

Other anatomical – identify bladder (urinary retention), biliary anatomy, including gallbladder (eg. acalculous cholecystitis), atelectasis, pneumothorax.

Nineteen out of twenty-six candidates passed this question.

Discussion

This question is identical to Question 2 from the first paper of 2008.

References

College Answer

There is still significant debate about the role of routine physiotherapy, but areas of physiotherapy
with their potential  benefit include:
•    Optimization of ventilation/respiratory function
•    Assistance in weaning
•    Advice on positioning of chest for improving ventilation
•    Joint protection
•    Minimise muscle damage, soft tissue injury
•    Muscle tone maintenance particularly in the neurological ICU patient
•    Early rehabilitation/mobilization
•    Liaison with medical and nursing staff

Potential risks/complications of physiotherapy techniques listed above include:
•    Deterioration in gas exchange
•    CVS instability
•    Barotrauma
•    Rise in ICP
•    Increased patient pain, stress and anxiety

Discussion

The role of physiotherapy is discussed in Question 24 from the second paper of 2013.

References

College Answer

Many problems are encountered after hospital discharge. The important problems include:
•    Patients have usually had a tracheostomy (and/or prolonged endotracheal intubation) - complications associated with these include laryngeal pathology [eg. polyps, ulcers], aspiration, difficulty with swallowing etc.
•    Limitation of mobility for some time – muscle tone, joint stiffness, Chronic Inflammatory
Polyneuropathy
•    Skin – hair loss, itching

•    Sexual dysfunction
•    Psychological problems – loss of memory, stress, nightmares, Post Traumatic Stress
Disorder, depression, chronic fatigue syndrome
•    Infectious: colonisation with resistant organisms (eg. MRSA)
•    Miscellaneous (loss of taste, loss of appetite, ocular trauma, scarring near region of tape fixing for ETT)
Tools to assess quality include: Quality Adjusted Life Years (objective measure), HAD – Hospital Anxiety & Depression, SF 36, PQOL (perceived quality of life), EuroQOL – European tool Simpler measures include Glasgow Outcome Scale. Some hospitals utilise follow up clinics. Eighteen out of twenty-six candidates passed this question.

Discussion

This question closely resembles Question 30 from the first paper of 2009.

References

College Answer

a)  Interventional techniques may be prophylactic (IVC filter to prevent PE) or therapeutic
(Eg)
1)  Coiling of an aneurysm
2)  Abscess drainage
3)  Embolisation of a bleeding vessel
4)  TIPS procedure for portal HT
5)  Angioplasty for vasospasm
6)  Coronary intervention

b)  May be as effective as surgery, but carry lower morbidity or mortality
Should be considered in ICU patients when the risk of more invasive procedures is greater

Limitations:
1)  Need to be performed in a radiology suite with all its limitations
2)  Might still need surgical back up if there is failure or if there is a complication
3)  Risk of contrast induced nephrotoxicity
4)  Complication specific for each interventional procedure

Discussion

This question is identical to Question 26 from the second paper of 2012.

References

College Answer

Assessment-

Severity of ulcer-superficial/deep The ulcer presents clinically as an
abrasion, blister, or shallow crater.

Signs of infection (systemic and local), contributing devices (eg splints, etc) Serial photographs          ·

Management-

Continue preventative strategies-

a) pressure relief through posture and regular (two hourly) turns and pressure relief devices (range of devices but can include foam/gel pads, special mattresses
b) Aim to mobilize (reduce/minimize any sedation) adequate analgesia for painful ulcers. Alert as high risk within ICU and determine tailored team approach.
c) Also treat/manage diarrhea and urinary incontinence.                  ·
d) Avoid·friction
e) Review unit protocols

Specific treatment

1) Dressings-occlusive or semipermeable dressing that will maintain a moi&t wound environment for superficial ulcers.
2) Infection-identify and treat accordingly
3) Surgery-ranging from minor removing infected granulation and necrotic tissue to major debridement
4) Adequate nutrition

Discussion

This question resembles a part of Question 2 from the first paper of 2003.

In the interest of revision, the answer is reproduced below. Additionally, LITFl have a nice section on pressure areas.

A structured approach would resemble the following:

Risk factors for pressure ulcers in ICU

A good article from 2000 has an exhaustingly long table (Table 1).

Highlights from this article include the following:

• Prolonged immobility
• Use of neuromuscular junction blockers
• Age over 60
• Severe illness (APACHE II score over 13)
• Hemodynamic instability preventing pressure area care
• Diabetes
• Incontinence
• Low albumin
• Poor nutrition
• Oedema
• Peripheral vascular disease
• Steroid use

Prevention of pressure ulcers in ICU

• Risk assessment and monitoring
• Mobility (may be unreasonable in this context)
• Minimise sedation and restraints to allow for self-repositioning (may not be relevan in this context)
• Management of incontinence
• 2 hourly repositioning
• Air mattress or specialised foam (evidence is not strong)
• Adequate skin care

Management of pressure ulcers in the ICU

• Engagement of a multidisciplinary wound care team
• Debridement
• Antibacterial (silver sulfadiazine) dressings
• Frequent dressing changes
• Exudate-absorbing dressings
• Promote wound healing:
  • Adequate nutritional supplementation, particularly of protein (2g/kg/day)
  • Control of diabetes
  • Avoidance of corticosteroids
  • Optimisation of tissue perfusion
  • Avoidance of oedema

References

Keller, Paul B., et al. "Pressure ulcers in intensive care patients: a review of risks and prevention." Intensive care medicine 28.10 (2002): 1379-1388.

Cullum, N., et al. "Beds, mattresses and cushions for pressure sore prevention and treatment." The Cochrane Library (2000).

REULER, JAMES B., and THOMAS G. COONEY. "The pressure sore: pathophysiology and principles of management." Annals of Internal Medicine94.5 (1981): 661-666.

Health Quality Ontario. "Pressure Ulcer Prevention: An Evidence-Based Analysis." Ontario health technology assessment series 9.2 (2009): 1.

Stratton, Rebecca J., et al. "Enteral nutritional support in prevention and treatment of pressure ulcers: a systematic review and meta-analysis." Ageing research reviews 4.3 (2005): 422-450.

Henzel, M. Kristi, et al. "Pressure ulcer management and research priorities for patients with spinal cord injury: consensus opinion from SCI QUERI Expert Panel on Pressure Ulcer Research Implementation." J Rehabil Res Dev 48.3 (2011): xi-xxxii.

Theaker, C., et al. "Risk factors for pressure sores in the critically ill."Anaesthesia 55.3 (2000): 221-224.

College Answer

a) Transport by any means involves risk to staff and patients 
b) Need to be familiar with the use of the transport vehicle~s 02~ suction, 
communications,and other equipment systems. 
c) Reduction in partial pressure of oxygen with altitude, critically ill patients who 
are already dependent on high Fi02 may be further compromised. 
d) Expansion of trapped gases-pneumothoraces~ intracranial air from injuries 
e) Expansion of air containing equipment - ET tube~ Sengstaken tube. ET cuff 
pressures will need to be adjusted 
f) IABP difficult to transport 
g) Risk of hypothermia 
h) As water partial pressure falls~ risk of dehydration through resp losses and 
passive humidification important 
i) Auscultation is difficult 
j) The ventilated patient is placed in the Trendelenburg and the reverse 
Trendelenburg positions during take off and landing respectively. This can 
impact on perfusion and oxygenation. 
k) Potential for pacemaker malfunction due to avionic interference. 
I) Staff doing air transport should refrain :from compressed. gas diving for at least 24 
hrs prior to transfer. . 
m) Physical problems: col~ noise, lighting, access to patient, motion sickness, 
acceleration injuries ( eg head to front of plane to avoid increased ICP on takeoff

Discussion

This question closely resembles Question 7 from the second paper of 2010.

References

College Answer

Daily “routine” CXR in (usually) intubated patients: controversial-evidence to support or refute practice, hard to study due to investigator bias, blinding problems and outcome assessment.

Generalisability may be an issue from often single specialty North American or European units to the usual multidisciplinary Australasian ICU. The consensus opinion of the Am. College of radiology is that daily routine CXR are indicated in patients who are mechanically ventilated . The evidence to date does not suggest that daily routine CXRs lead to changes in therapeutic decision making. Data suggest that length of stay and duration of mechanical ventilation are not adversely affected by elimination of daily routine CXR.

Benefits:

a) Confirmation of placement of major lines / tubes / pipes / wires

detects expected/unexpected disease progression/complications requiring treatment

b) Reasonable assessment of hypervolaemia/LVF, new infiltrates accompanying fever, pleural complications, endotracheal tube displacement

Problems:

radiation exposure-staff/patients potential for line/tube displacement Cost

False positive/false negative findings

Discussion

Rationale for routine CXRs:

• Critically ill patients may have rapidly evolving thoracic pathology
• This pathology may not be easily evaluated by clinical means
• Mechanically ventilated patients are especially prone to rapid changes
• Routine radiography may yield a management-influencing surveillance benefit

Advantages:

• Regular review of line and tube position
• Regular review of fluid balance as observed by pulmonary interstitial water
• Surveillance for VAP
• Assessment of the reasiness for extubation
• Observation of changes in lung parenchyma in response to treatment (eg. resolution of pneumonia)

Disadvantages:

• Radiation exposure
• Risk of tube/line dislodgement with positioning
• Lack of association between radiological apparance and physiological performance

Evidence and recommendations:

• Only about 7% of CXRs result in a change in management
• In another study, only 2.3% of CXRs revealed new pathology
• 2012 meta-analysis: no harm associated with "restrictive" use of CXRs
• Americal College of Radiology recommends they are performed for clinical indications only

References

Ganapathy, Anusoumya, et al. "Routine chest x-rays in intensive care units: a systematic review and meta-analysis." Crit Care 16.2 (2012): R68.

Amorosa, Judith K., et al. "ACR appropriateness criteria routine chest radiographs in intensive care unit patients." Journal of the American College of Radiology 10.3 (2013): 170-174.

Veličković, Jelena, et al. "Routine chest radiographs in the surgical intensive care unit: Can we change clinical habits with no proven benefit?." Acta chirurgica iugoslavica 60.3 (2013): 39-44.

Cruz, Jeffrey, et al. "Evaluation of the Clinical Utility of Routine Daily Chest Radiography in Intensive Care Unit Patients With Tracheostomy Tubes A Retrospective Review." Journal of intensive care medicine (2014): 0885066614538393.

College Answer

Multisystem issues;

CVS: High prevalence of cardiac disease, CAD, silent ischemia, less responsive to symathetic stimulation and therefore lesser response to catecholamines, greater diastolic dysfunction and conducting system disease, likelihood of being on cardiac drugs. ( 3 marks)

RS: Swallow dysfunction- risk of aspiration

Decreased ventilatory response to hypoxia and hypercapnia

Decreased chest wall complance, muscle strength and increase in closing volume.

Renal: Decrease in renal function, lower muscle mass so a serum creatinine at the upper end of normal may indicate renal failure

Metabolic: Reduced BMR, risk of overfeeding

CNS: Higher incidence of delirium, age related loss of cerebral volume

Drug dosing: Altered pharmacokinetics, reduced renal and hepatic reserve, need dose adjustment, increased sensitivity to sedation and analgesia

Greater operative morbidity and mortality

Discussion

This question closely resembles a part of Question 9 from the first paper of 2012. To simplify revision, parts of that answer are reproduced below. However, the college answer does not seem to answer the college question. The question asked for age related factors which adversely affect outcome ; the college answer instead went on to discuss age-related changes in physiology, and how these influence intensive care management.

Let us talk about the outcomes first.

Influence of age:

• Mechanical ventilation : in-hospital mortality among octogenarians  = 70%
• If the reason for ventilation was pneumonia, in-hospital mortality for the over-65s = 62%
• In hospital mortality for octogenarians admitted with sepsis = 85%
• In brain injury, risk of death or disability is doubled in the elderly.

Influence of functional status and co-morbidities:

• Functional dependence: in-hospital mortality = 30% (vs.  7.8% if independent)
• Dementia: mortality = 55.9%  versus 8.2% in those without cognitive impairment.
• Delirium: independent predictor of reintubation, prolonged hospital stay and mortality.
• Malnutrition: low BMI increases mortality in the elderly.

Expected functional outcome:

• Only 14% of patients aged 85 years or older went home without home health care.
• After discharge, mortality occurred predominantly during the first 3 months. If you survive ninety days, you're probably going to be ok.
• Many elderly patients do not want intensive care. "In a population of patients with limited life expectancy and aged 60 years or older, 74% stated that they would not choose treatment if the burden of treatment were high and the anticipated outcome survival with severe functional impairment".

Now; how does old age influence intensive care management?

Changes in airway management:

• Intubation may be easier due to the patient being edentulous
• Intubation may be more difficult due to C-spine and TMJ arthritis
• Bag-mask ventilation may be more difficult because of missing teeth and wasting of facial soft tissues
• Swallowing may be impaired and aspiration is more likely
• Mechanisms maintaining airway patency are impaired, and extubation failure is more likely
• Greater risk of post-induction cardiovascular collapse

Changes in respiratory management and ventilation

• Decrease in expectations: SpO₂ goals may be lowered (~ 92%, due to "senile emphysema")
• Chest physiotherapy becomes more important (decreased respiratory muscle strength)
• Early extubation is favoured (to prevent deconditioning)
• There is decreased sensitivity of respiratory centres to hypoxia and hypercapnia, which must be considered.

Changes in approach to cardiovascular support

• Responsiveness to β-adrenergic receptor stimulation is decreased; higher doses of vasopressors may be required
• Baroreceptors and chemoreceptors are less reactive
• Levels of circulating catecholamines are increased
• An increased blood pressure goal is therefore appropriate when titrating vasopressors: chronic hypertension is almost assured, and with this, organ bloodflow autoregulation is impaired (i.e. more closely tied to pressure).

Changes in assessment of neurological function

• Increased risk of delirium (therefore, greater vigilance in screening for delirium)
• Decreased expectation of neurological performance, eg. when assessing for extubation (pre-existing dementia)
• Parkinson disease (unusual response to antidopaminergic drugs)
• Pre-existing weakness may produce a "difficult to wean" scenario

Changes in approach to the support of renal function

• Age-related decrease in GFR is to be expected
• Renal blood flow decreases; the kidneys are more susceptible to fluctuations of blood pressure
• Renal blood flow autoregulation undegoes a left-shift; thus a higher perfusion pressure may be required (eg. a MAP of 75-80)
• Because of these factors, old kidneys are more susceptible to dialysis-associated renal dysfunction. This influences the decision as to whether one does or does not offer dialysis.

Changes in approach to nutrition

• Albumin is expected to be low (due to age-related decrease in albumin synthesis)
• Decreased glycogen reserve means greater vigilance in monitoring for hypoglycaemia
• Decreased metabolic rate means nutritional requirements may be lower than predicted by crude approximations of caloric requirements
• Likelihood of premorbid malnutrition is greater - thus, more susceptible to refeeding syndrome

Changes in approach to blood transfusion

• Age-related hanges in haematological function influence your expectations: these patients are more likely to be chronically anaemic, and well adapted to anaemia.
• Decreased marrow cellularity results in a diminished response to anaemia and EPO.
• Chronic anaemia of malnutrition may pre-date ICU admission

Changes in interpetation of the clinical features of sepsis

• There is diminished immune response, both cellular and humoural.
• The elderly may not mount a febrile response, and may actually be hypothermic with sepsis
• Decreased synthetic function of the liver may result in diminished synthesis of CRP

Changes in pharmacology

• Drug levels may not represent the effective "free" fraction due to changed in protein binding and volume of distribution
• Dose adjustments need to be made to accoun

References

Solh, Ali A. El, et al. "Extubation failure in the elderly." Respiratory medicine 98.7 (2004): 661-668.

Linton, Phyllis Jean, and Kenneth Dorshkind. "Age-related changes in lymphocyte development and function." Nature immunology 5.2 (2004): 133-139.

Muschler, George F., et al. "Age‐and gender‐related changes in the cellularity of human bone marrow and the prevalence of osteoblastic progenitors." Journal of Orthopaedic Research 19.1 (2001): 117-125.

Grady, C. L., et al. "Age-related changes in brain activity across the adult lifespan."Cognitive Neuroscience, Journal of 18.2 (2006): 227-241.

de Rooij, Sophia E., et al. "Factors that predict outcome of intensive care treatment in very elderly patients: a review." Critical Care 9.4 (2005): R307.

College Answer

1) Sepsis – It is now believed that genetic predisposition influences the risk of serious infection and outcome from severe injury. These genetic variations are thought to be the result of single nucleotide polymorphisms (SNP). These are thought to influence the severity of injury by controlling the induction of TNF, NF kappa B and toll receptors. Some examples include polymorphisms in TLR 2, 4 and 5 genes, CD14 and mannose binding lectin genes.

2) Acute lung injury The genetic susceptibility to the development of and variable outcomes in acute lung injury/acute respiratory distress syndrome (ALI/ARDS) has become a topic of great interest in the pulmonary and critical care community. Published studies of variable genetic susceptibility to ALI/ARDS already have identified some important candidate genes and potential gene-environment interactions. Some examples include variant alleles in Mannose binding lectin genes and surfactant protein B gene polumorphism.

3) Head injury – There is now data to suggest that the presence of certain Apo
Lipoprotein genes may have an adverse outcome in head injury.

4) Pharmacogenomics: Response to and adverse effects of a drug are thought to have a genetic basis

5) IHD, CVA also have some genetic basis.

Discussion

In brief, the following specific associations between genotype and response to critical illness have been found:

• Risk of developing MODS from acute pancreatitis is influenced by TNF-α gene variants (Bishehsari et al, 2012)
• Risks of developing ARDS in community acquired pneumonia is related to genes encoding proteins A and D of pulmonary surfactant (García-Laorden et al, 2011)
• Susceptibility to sepsis (and to death from sepsis) seems to be related to a whole host of genetic variations, specifically in the genes encoding interleukin (IL)-1 receptor antagonist gene, the heat shock protein gene, the IL-6 gene, the IL-10 gene, the CD-14 gene, the Toll-like receptor (TLR)-4 gene, and the TLR-2 gene (Holmes et al, 2003)
• Delirium in critical illness is associated with a apolipoprotein E4 polymorphism (Ely et al, 2007)
• Outcome in brain injury seems to be worse for people featuring the apolipoprotein E-ε4 genotype (Friedman et al, 1999)

In addition, the following comorbidities feature significantly in ICU outcomes, and have a known genetic basis:

• NIDDM
• IHD
• Emphysema (α-1 antitrypsin deficiency)
• Cerebrovascular disease
• Various genetic disorders and sporadic mutations / chromosomal abnormalities; of which some notable examples are Down syndrome, which results in congenital cardiac defects, and Prader-Willi, which is associated with OSA and obesity hypoventilation syndrome.

References

Chung, T. Philip, et al. "Functional genomics of critical illness and injury." Critical care medicine 30.1 (2002): S51-S57.

Villar, Jesús, et al. "Bench-to-bedside review: understanding genetic predisposition to sepsis." Critical Care 8.3 (2004): 180.

Ely, E. Wesley, et al. "Apolipoprotein E4 polymorphism as a genetic predisposition to delirium in critically ill patients*." Critical care medicine 35.1 (2007): 112-117.

Bion, J. F. "Susceptibility to critical illness: reserve, response and therapy."Intensive care medicine 26.1 (2000): S057-S063.

Bishehsari, Faraz, et al. "TNF-alpha gene (TNFA) variants increase risk for multi-organ dysfunction syndrome (MODS) in acute pancreatitis." Pancreatology 12.2 (2012): 113-118.

García-Laorden, M. Isabel, et al. "Influence of genetic variability at the surfactant proteins A and D in community-acquired pneumonia: a prospective, observational, genetic study." Crit Care 15.1 (2011): R57.

Holmes, Cheryl L., James A. Russell, and Keith R. Walley. "Genetic polymorphisms in sepsis and septic shock: role in prognosis and potential for therapy." CHEST Journal 124.3 (2003): 1103-1115.

Ely, E. Wesley, et al. "Apolipoprotein E4 polymorphism as a genetic predisposition to delirium in critically ill patients*." Critical care medicine 35.1 (2007): 112-117.

Friedman, G., et al. "Apolipoprotein E-ε4 genotype predicts a poor outcome in survivors of traumatic brain injury." Neurology 52.2 (1999): 244-244.

College Answer

Presence of a notch – spleen
Spleen moves inferomedially on inspiration
Not ballotable or bimanually palpable
Usually no band of resonance over s splenic mass
Spleen has no palpable upper border
Dullness over ribs 9,10, 11

Discussion

This is another question which reaches into a deep dark recess of Talley and O'Connor.

The differences between spleens and kidneys are mobility, ballotability, and edge palpation.

• Thus, the spleen is mobile with respiration, whereas the kidneys is not.
• The kidney is "ballotable" whereas the spleen is not.
• The spleen has a notch on the anterior surface, and the kidney does not
• The spleen should be dull to percussion, where the kidney can be resonant due to overlying gas
• The spleen enlarges diagonally, towards the umbilicus and the RLQ, whereas the kidney enlarges inferiorly, to the ipsilateral pelvis.
• There is no palpable upper border to the spleen, whereas the kidney should have one

The reference for the above wisdom, shamefully, is Wikiversity.

References

College Answer

Causes:

1) Environment: Noise, light, Patient care activities (monitoring, positioning, suction etc) (These only account for 30%)

2) Pharamacological – use of benzodiazepines and narcotics

3) Gravity of illness

4) IPPV

5) Any pre-existing cause of sleep disturbance

In a large proportion, cause of disordered sleep unknown

Consequences:

1)  Delirium (this has an adverse effect on long term outcome).

Treatment

1)  Minimising noise (ear plugs)

2)  Cut down lights

3)  Optimal ventilatory parameters to avoid non-triggered breaths, avoiding apnoeas and episodes of desaturation

4)  Atypical antipsychotics

5)  Role of melatonin – needs evaluation

Discussion

This topic has been of some considerable interest, considering how many articles pop up when you look up "sleep disturbance in the ICU". Much of this information has been derived from this excellent article from the The Open Critical Care Medicine Journal:

The following factors have been found to act as negative influences:

• Noise: 10-20% of wakings
• Constant harsh light; misalignment of circaian cycles - artificiasl light is of insufficient intensity to act as a zeitgeber
• Sunlight exposure is limited or nonexistant
• Erratic stimulus (eg. hourly neuro obs)
• Appropriately timed meals are replaced by tube feeding
• Regular nursing care (eg. turns) disturbs nocturnal sleep
• Sepsis decreased REM sleep by influencing melatonin secretion
• Sedatives impair normal REM sleep
• Mechanical ventilation impairs sleep

The EPA recommends no higher than 45 dB in the ICU; however, this is actually quite loud - it is "the sound level recognized internationally as an upper limit for human comfort in residential interior spaces".

The following consequences have been ascribed to sleep deprivation, though in truth there really is no way of testing that.

• Delirium
• Impaired immunity
• Increased use of sedatives
• Impaired sleep following sicharge from ICU

Management of sleep disturance in the ICU:

• Noise minimisation
• Light level fluctuation to model the day-night rhythm
• Minimisation of mechanical ventilation, and the use of patient-triggered modes
• Atypical antipsychotics for delirium
• Use of melatonin (the studies are too few, and too heterogeneous, to make recommendations at this stage)

References

Wang, Janice, and Harly Greenberg. "Sleep and the ICU." Open Critical Care Medicine Journal 6.1 (2013): 80-87.

Schwab, Richard J. "Disturbances of sleep in the intensive care unit." Critical care clinics 10.4 (1994): 681-694.

Langevoort, G., et al. "Sleep disturbances in the ICU." Critical Care 15 (2011): 1-190.

Parthasarathy, Sairam, and Martin J. Tobin. "Sleep in the intensive care unit."Applied Physiology in Intensive Care Medicine 2. Springer Berlin Heidelberg, 2012. 61-70.

Bellapart, J., and R. Boots. "Potential use of melatonin in sleep and delirium in the critically ill." British journal of anaesthesia 108.4 (2012): 572-580.

College Answer

a)  Describe four (4) abnormalities visible in this patient’s hand.
•    Ulnar deviation
• Wasting of dorsal interosseous muscles
• Boutoniere deformity of index and middle finger
•    Subluxation at metacarpal-phalangeal joints
• Z-deformity of thumb

b)  What is the most likely diagnosis?
• Rheumatoid arthritis

c)  List three (3) associated abnormalities that may complicate intubation in patient’s with this condition?
• Arthritis of tempero-mandibular joint -> limited mouth opening
• Atlanto-axial subluxation -> spinal cord injury possible
• Degenerative arthritis in C-spine -> difficult visualisation of larynx
• Laryngeal arthritis -> poor vocal cord opening
• Pulmonary fibrosis -> poor respiratory reserve

Discussion

Rheumatoid hands make an appearance in Question 10.3 from the second paper of 2013.

In general, the clinical features of rheumatoid arthritis include the following:

• Symmetric joint swelling, MCP > DIP
• Morning stiffness  lasting at least 1 h before maximal improvement 
• Extra-articular synovitis (tenosynovitis, bursitis)
• General symptoms (malaise, fatigue, weight loss, fever)
• Hand signs as mentioned above:
  • Ulnar deviation
  • Z deformity of the thumb
  • Swan neck deformities
  • Swelling of metacarpo-phalangeal joints
  • Wasting of small muscles of the hand
  • Boutonnieres deformity

The site clinicalexam.com has an excellent entry on RA, with extensive lists of signs and examination techniques.

The rest of this question would benefit from a structured answer.

An article on anaesthetic considerations in RA has a niic etable (Table 2) of extra-articular manifestations of rheumatoid arthritis.

The following features of RA act as influences in the critical care of these patients

1. Difficult intubation, as caused by the abovementioned issues:
   1. Poor neck extension due to C-spine arthritis
   2. Risk of spinal cord injury due to atltantoaxial subluxation
   3. Poor mouth opening due to TMJ arthritis
   4. Poor vocal cord opening due to laryngeal arthritis or crico-arytenitis
   5. Poor respiratory reserve due to pulmonary fibrosis
   6. Difficulty assessing all of these issues in the context of an ICU intubation - you are not seeing this person in the pre-admission clinic; likely they are trying to die in some sort of advanced life support scenario.
2. Difficult mechanical ventilation:
   1. Oxygenation pproblems:
      1. Pulmonary fibrosis, diffusion defect
      2. Pulmonary hypertension
   2. Ventilation problems
      1. Pleural effusions
      2. Restrictive lung disease with poor complicance
   3. Weaning problems:
      1. Poor muscle strength due to steroid myopathy
      2. Delayed extubation if the intubation was difficult
3. Cardiac and vascular problems:
   1. Propensity to arrhythmias
   2. Increased risk of ischaemic heart disease
   3. Diastolic failure due to restrictive cardiomyopathy and pericardial disease make fluid resuscitation challenging
   4. Cardiac weirdopathy (eg. failure due to amyloid deposition needs to be considered in the differential diagnosis of an otherwise unexplained heart failure when the patient also has RA)
   5. Difficult vascular access (limb deformities)
   6. Poor mobility and deformity promotes the development of pressure areas
4. Neuropsychiatric problems:
   1. Steroid-induced psychosis - extubation may be interesting
   2. Psychological problems of chronic disease
   3. Increased analgesic requirements (chronic opiate/NSAID use)
5. Electrolyte and endocrine abnormalities associated less with RA than with its treatment:
   1. Chronic steroid use may promote hypoadrenalism
   2. Electrolyte derangement due to chronic steroid use
6. Renal problems:
   1. RA-associated (eg. glomerulonephritis, amyloidosis)
   2. Treatment-associated (eg. NSAID-induced damage)
   3. Does one commit to long term dialysis in this setting?
7. Gastrointestinal and nutritional problems:
   1. "Rheumatoid cachexia" due to cytokine-driven hypermetabolism promotes the need for more protein and calories (Roubenoff et al, 1994) - but it is unclear whether they benefit from "overfeeding", as they tend to become cachexic in spite of a theoretically adequate dietary intake.
   2. Gastic erosion/ulceration due to chronic steroid and NSAID use suggests that this group should get PPIs routinely
8. Haematological disturbances
   1. Anaemia of chronic disease: will you transfuse them?
   2. Thrombocytopenia (Felty's) - increased risk from neuraxial procedures and vascular access
9. Immune and infectious issues
   1. Increased risk of infection
   2. Increased propensity to be often seen in hospitals tends to result in increased risk of MRO colonisation
   3. Weird antiRA drugs may interact with antibiotics

References

Canelli, Robert, John P. Weaver, and Elifce Cosar. "Anesthetic Considerations for Cervical Fusion Surgery in Advanced Rheumatoid Arthritis and Severe Pulmonary Hypertension." (2012).

McInnes, Iain B., and Georg Schett. "The pathogenesis of rheumatoid arthritis." New England Journal of Medicine 365.23 (2011): 2205-2219.

Samanta, R., K. Shoukrey, and R. Griffiths. "Rheumatoid arthritis and anaesthesia."Anaesthesia 66.12 (2011): 1146-1159.

College Answer

Roles include –

Cardiac echo – be it transthoracic or transoesophageal looking at structure, function, relationships between the two ventricles and pericardial effusions. Doppler cardiac output monitoring – oesophageal, transthoracic

Vascular – specifically thoracic aorta – but also abdominal aorta. Other vascular include any accessible artery (eg radial, brachial, femoral, carotid etc), grafts for flow assessment, stenosis, patency. Also veins – for thrombosis/patency

Cranial – monitor cerebral blood flow hyperaemia, ischaemia, brain death, detection of vasospasm, fat and other emboli, stroke related artery reperfusion following thrombolysis.

Other –pleural, diaphragm etc

Diagnostic ultrasound, esp abdomen – identify bladder (urinary retention), biliary anatomy, including gallbladder important to mention acalculous cholecystitis, atelectasis, pneumothorax

Ultrasound assisted interventions (drainage of collections)

Vessel identification for line insertion

Discussion

A nice article about the use of ultrasound in the ICU can be found in Continuing Education in Anaesthesia, Critical Care & Pain (Wilson and Mackay, 2012).

This question can be approached systematically; the answer presented below has been modelled on Table 1 from this article, and is organised by body area being examined:

• Head:
  • Transcranial doppler in SAH-associated vasospasm and in confirmation of brain death
• Neck
  • Central line insertion
• Thoracic
  • Identification of pneumothorax
  • Localisation and ultrasound-guided aspiration of pleural effusions
• Cardiac
  • Echocardiography (structure and function)
  • Ultrasound-guided pericardiocentesis
• Abdominal
  • FAST
  • Solid organ pathology (eg. hydronephrosis, splenomegaly, cirrhosis)
  • Renal vascular flow
  • Gall bladder pathology
  • Portal vein pathology
  • Aortic pathology
• Peripheral
  • Peripheral venous access
  • Peripheral arterial flow assessment
  • Assessment of DVTs

References

Wilson, Stephen, and Andrew Mackay. "Ultrasound in critical care." Continuing Education in Anaesthesia, Critical Care & Pain 12.4 (2012): 190-194.

College Answer

      A daily interruption of sedation may have a role in preventing over-sedation and reducing the duration of mechanical ventilation in selected mechanically ventilated ICU patients. (a reasonable opening summary statement)

Evidence:

There are two clinical trials of interruption of sedation that show
o significant reduction in duration of ventilation (0.5)
o duration of ICU stay (0.5)
o fewer CNS investigations. (0.5)
•    Follow up studies suggested that there was a decrease in a range of complications including:
•     VAP, Upper GIT haemorrhage, bacteraemia, venous thromboembolic disease and sinusitis) in patients who received a daily interruption of sedation. (1)
•    There is also a single observational study of longer term outcomes that suggests that a daily scheduled interruption of sedation is not associated with worse psychological outcomes. (0.5)

Candidates were awarded extra  marks  if they mentioned he names of the two big RCTs or if they offered a critical appraisal  of the most recent evidence.
o   Kress 2000 NEJM
and
o   Girard, Lancet 2008 or Awake and Breathing Controlled (ABC) study
o   Critical appraisal of the Girard RCT: appropriate randomisation with
allocation concealment, intention to treat analysis, unblinded

Potential problems:

Routine daily interruption of sedation is not appropriate for all patients, for example;
•    Those with poorly controlled intracranial pressure
•    Those requiring controlled ventilation
•    Those in whom self extubation is particularly dangerous (e.g., those intubated for airway obstruction)
•    Those patients receiving therapy that is likely to be particularly distressing (burns, permissive hypercapnia

Summary statement

•     Due to the risks involved, particularly the risk of self-extubation (10% is a lot!) the use of the protocol would need to be adapted to local circumstances. Studies to date have been performed in the USA. It could be disastrous if a patient self- extubated when there were not sufficiently skilled personnel available to
appropriately manage the patient’s airway.  Thus “routine” daily interruption may not be necessary if the ICU is closed and the level of sedation required is assessed daily by skilled and knowledgeable staff.

Discussion

This question is identical to Question 1 from the first paper of 2013.

References

College Answer

General risks of MRI

Magnetic field induced movement of ferromagnetic objects

* Ferrous Projectiles accelerating into scanner causing trauma

* Movement of ferrous implants and prostheses

* Movement of metallic foreign bodies, such as foreign bodies in the eye

Others 
* Malfunction/failure of pacemaker/ IAD

Specific risks with the critically ill patient
* Cold environment and prolonged exposure time away from ICU due to length of time it takes to do an MRI

* Patient inaccessibility

* Monitoring and ventilation equipment is limited and needs to be MRI compatible, often sub-optimal

* Unable to take resuscitation equipment into “magnet zone”

* Infusions may be difficult to run – MRI compatible pumps that can be used in “magnet zone” are not widely available. Long tubing can be used.

* Gadolinium exacerbation of nephrogenic systemic fibrosis

Potential risk of hyperthermia in patients with disordered thermal regulation (ie all critically ill patients)

Potential for burns (ECG dots)

Discussion

Even though the college exclude transportation considerations from their question, they are important because according to one risk/cost/benefit analysis, "transportation of patients from the ICU resulted in a large number of physiologic changes, each requiring changes in support". Of these physiologic changes, 68% were described as "serious" (eg. requiring more vasopressors or a higher FiO₂).

Now, to MRI issues. This article contains a chapter ("MRI Transport") which covers this topic in brief. A substantial detailed exploration can be found in David Olive's article for Australasian Anaesthesia(2005)

Risks from the magnet

• Ferromagnetic material movement
• Malfunction of pacemakers
• Projectile trauma from nearby objects
• Cardiac damage from PA catheters
• Pulse oximeters and ECG dots can overheat and cause burns. ECG cables are made of coiled copper, and will also heat up.

Risks from contrast

• Gadolinium is usually quite safe, but it may cause exacerbation of nephrogenic systemic fibrosis. Anaphylactic reactions are possible.

Risks from the isolated room

• Airway disconnection alarms might go unheard
• Long ventilator tubing creates excessive amounts of dead space
• Extra dead space makes is difficult to trigger.
• MRI-compatible anaesthetic machines are available, but they are expensive (~ $80,000) and frequently the ventilators on them are somewhat unsophisticated.
• Long infusion tubing results in a delay of medication administration
• Some drugs may require pumps, and cannot be given; pumps may require ridiculously long tubing and additional batteries to function
• The MRI chamber is usually cold, and hypothermia can develop
• Monitoring equipment is of poor quality

Risks from being critically ill

• Thermoregulation is impaired, and hypothermia is more likely to develop
• Judgement is impaired, and patient movement delays the process
• Resuscitation equipment cannot be taken into the room. Certainly, plastic disposable laryngoscopes do exist, but the batteries inside them are still affected.
• If cardiac arrest occurs, it can take some time to dismount the MRI couch

References

INDECK, MATTHEW, et al. "Risk, cost, and benefit of transporting ICU patients for special studies." Journal of Trauma-Injury, Infection, and Critical Care 28.7 (1988): 1020-1025.

Tobin, J. R., E. A. Spurrier, and R. C. Wetzel. "Anaesthesia for critically ill children during magnetic resonance imaging." British journal of anaesthesia69.5 (1992): 482-486.

Blakeman, Thomas C., and Richard D. Branson. "Inter-and Intra-hospital Transport of the Critically Ill." Respiratory care 58.6 (2013): 1008-1023.

ANZCA have an excellent college publication on this exact topic:

D.Olive, "Don't Get Sucked in: Anaesthesia for Magnetic Resonance Imaging" - Australasian Anaesthesia 2005, pp.85

College Answer

a) 
•    Evidence of Raynaud’s or ischaemia with pallor of digits,
•     Sclerodactaly 
•     Calcinosis, 
•    Multiple amputations of distal digits
•    Distal ulceration with gangrene
•    Fixed flexion deformity of ring finger right hand.

b)     Systemic sclerosis or Scleroderma

c) 
•    Telangiectasia, 
•    Fine creps bibasally due to lower lobe fibrosis,
•    Beaking of the nose
•    Limitation of mouth opening
•    Thickening of the skin and pigmentation changes
•    Features consistent with Pulmonary H/T,
•    Sjogrens syndrome
•    Oesophageal involvement
•    Renal failure

Discussion

Scleroderma is also the subject of Question 28 from the first paper of 2012, but the information requested there is rather different.

Who cares if the hands don't demonstrate all the signs in the college answer? The cutaneous manifestations of scleroderma are as follows:

• Skin thickening
• Oedema of the digits
• Sclerodactyly
• Pitting ulceration, particularly at the fingertip
• Calcinosis over joints
• Telangiectasia
• Raynauds phenomenon

Other clinical features:

• Sjogren syndrome
• difficult intubation (limited mouth opening)
• Pulmonary fibrosis, restrictive lung disease, pulmonary hypertension
• Cardiac arrhythmias, myocardial fibrosis, pericardial stricture
• Corticosteroid-associated psychosis; chronic fatigue
• hyponatremia and fluid retention due to corticosteroid therapy
• renal failure, renal artery stenosis
• Oesophagitis, poor gut motility, decreased feed tolerance, risk of aspiration
• Difficult vascular access
• Immunosuppressive therapy leading to increased infection risk

References

Farber, Harrison W., Robert W. Simms, and Robert Lafyatis. "Analytic Review: Care of Patients With Scleroderma in the Intensive Care Setting." Journal of intensive care medicine 25.5 (2010): 247-258.

Legerton 3rd, C. W., Edwin A. Smith, and Richard M. Silver. "Systemic sclerosis (scleroderma). Clinical management of its major complications."Rheumatic diseases clinics of North America 21.1 (1995): 203-216.

TUFFANELLI, DENNY L., and R. K. Winkelmann. "Systemic scleroderma: a clinical study of 727 cases." Archives of Dermatology 84.3 (1961): 359-371.

Silver, Richard M. "Clinical aspects of systemic sclerosis (scleroderma)." Ann Rheum Dis 50.suppl 4 (1991): 854-61.

In order to replace the college photograph, I have had to misappropriate a series of images from various sites:

The first set of (ulcerated) hands are from Health in Plain English;

The hands with digital pallor and telangiectasia are from... I can't remember where. Google?

The final set of digits with amputations and calcinosis are from Pathguy. Thank you, Pathguy!

College Answer

a)  The rash is
•     Erythematous, 
•     Patchy 
•     Widespread 
•    Bullous formation or blistering

b)  Top 3 differentials
•    Stevens – Johnson syndrome (erythema multiforme major)
•    Drug eruption
•    Bullous pemphigoid

Less likely, but worthy of some marks
•    Staphyloccocal scalded skin syndrome
•    Toxic shock syndrome
•    Purpura fulminans

c) 
•    history in particular recent drug exposure, other symptoms of infective aetiology, Exposure to infected children
•    FBC, UEC, LFTs, CRP, COAGs
•    Serology – Mycoplasma and varicella
•    Skin biopsy
•    Blood cultures
•    MC&S of bullae

Discussion

This question closely resembles Question 15.1 from the second paper of 2012. Like all "name that rash" questions, this one suffers massively from the loss of the official college photograph.

So, in lieu of a sensible list of differentials, here is a list of random differentials for a severe generalised rash of uncertain aetiology:

Vascular causes:

• Shower of emboli
• Vascular insufficiency

Infectious causes:

• Toxic epidermal necrolysis
• Staphylococcal scalded skin syndrome
• Viral exanthem/manifestations of viral infection
• Fungal infection eg. candida

Neoplastic causes:

• Cutaneous lymphoma/leukaemia

Drug-related causes

• Stevens Johnson syndrome
• Red Man syndrome (vancomycin)

Autimmune cause

• Allergic reaction
• Vasculitis
• Erythema multiforme
• Graft-versus-host disease

Traumatic causes

• Burns

The standard work-up:

• FBC for eosinophilia
• Viral serology for HSV, VZV, HIV, EBC, CMV
• Culture of exudate
• Mycoplasma serology
• Vasculitic screen
• Skin biopsy

References

College Answer

°     Inflammatory bowel disease

°     Thyrotoxicosis

°     Idiopathic

°     Familial

°     Cirrhosis

°     Celiac

°     Pregnancy

Discussion

There are numerous causes of clubbing.

Here is an unreasonably long list:

Causes of bilateral clubbing in both hands and feet

Cardiac

• Congenital heart disease, particularly cyanotic defects
• Congestive cardiac failure
• Aortic aneurysm
• Subacute bacterial endocarditis
• Arteriovenous fistula (and it would have to be a major one)

Respiratory

• Chronic lung disease of any sort, really;
  • Bronchiectasis, which makes you think of cystic fibrosis
  • COPD, asbestosis
  • Pulmonary fibrosis of any aetiology
  • Empyema which has been going on for a while
• Lung carcinoma (according T and O’C, usually not the small-cell variety)

Gastrointestinal

• Cirrhosis; for some reason, particularly primary biliary cirrhosis
• Coeliac disease
• Inflammatory bowel disease
• Malignancy of the colon

Uncommon causes of clubbing

• Thyrotoxicosis
• Pregnancy
• Syringomyelia
• Hyperparathyroidism
• Pregnancy
• Inherited familial (some people are just born that lucky – it’s a Mendelian dominant trait)

Causes of clubbing in feet only

• Coarctation of aorta
• Abdominal aortic aneurysm

Causes of unilateral clubbing 

• Any sort of arterial aneurysm leading into the clubbed limb
• Apical lung tumour
• Hemiplegia

References

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where. Get your own.

Rutherford, John D. "Digital Clubbing." Circulation 127.19 (2013): 1997-1999.

Velur, Prasuna, and Giridhar P. Kalamangalam. "Teaching NeuroImages: Unilateral clubbing in hemiplegia." Neurology 78.19 (2012): e122-e122.

Stoller, James K., et al. "Reduction of intrapulmonary shunt and resolution of digital clubbing associated with primary biliary cirrhosis after liver transplantation." Hepatology 11.1 (1990): 54-58.

Dickinson, C. J., and J. F. Martin. "Megakaryocytes and platelet clumps as the cause of finger clubbing." The Lancet 330.8573 (1987): 1434-1435.

College Answer

a) What complication has developed?
Pressure area ulcer

b) What are the risk factors for this complication?
Duration of surgery, faecal incontinence and/or diarrhoea, low albumin concentrations, disturbed 
sensory perception, obesity, moisture of the skin, impaired circulation, use of inotropic drugs, diabetes mellitus, too unstable to turn, decreased mobility, and high APACHE II score. Waterlow’s score, or other valid scores

c) What is the management of this complication?
Remove all pressure from area, appropriate wound management, plastic surgical review, and
adequate nutrition. Wound nurse team.

d) What are the major preventative strategies for this complication in intensive care patients? Maintaining clean and dry skin, visualise skin integrity twice a day, regular pressure relief, pressure relief mattresses

Discussion

This question closely resembles a part of Question 2 from the first paper of 2003. To simplify revision, the answer is reproduced here.

Risk factors for pressure ulcers in ICU

A good article from 2000 has an exhaustingly long table (Table 1).

Highlights from this article include the following:

• Prolonged immobility
• Use of neuromuscular junction blockers
• Age over 60
• Severe illness (APACHE II score over 13)
• Hemodynamic instability preventing pressure area care
• Diabetes
• Incontinence
• Low albumin
• Poor nutrition
• Oedema
• Peripheral vascular disease
• Steroid use

Prevention of pressure ulcers in ICU

• Risk assessment and monitoring
• Mobility (may be unreasonable in this context)
• Minimise sedation and restraints to allow for self-repositioning (may not be relevan in this context)
• Management of incontinence
• 2 hourly repositioning
• Air mattress or specialised foam (evidence is not strong)
• Adequate skin care

Management of pressure ulcers in the ICU

• Engagement of a multidisciplinary wound care team
• Debridement
• Antibacterial (silver sulfadiazine) dressings
• Frequent dressing changes
• Exudate-absorbing dressings
• Promote wound healing:
  • Adequate nutritional supplementation, particularly of protein (2g/kg/day)
  • Control of diabetes
  • Avoidance of corticosteroids
  • Optimisation of tissue perfusion
  • Avoidance of oedema

References

Keller, Paul B., et al. "Pressure ulcers in intensive care patients: a review of risks and prevention." Intensive care medicine 28.10 (2002): 1379-1388.

Cullum, N., et al. "Beds, mattresses and cushions for pressure sore prevention and treatment." The Cochrane Library (2000).

REULER, JAMES B., and THOMAS G. COONEY. "The pressure sore: pathophysiology and principles of management." Annals of Internal Medicine94.5 (1981): 661-666.

Health Quality Ontario. "Pressure Ulcer Prevention: An Evidence-Based Analysis." Ontario health technology assessment series 9.2 (2009): 1.

Stratton, Rebecca J., et al. "Enteral nutritional support in prevention and treatment of pressure ulcers: a systematic review and meta-analysis." Ageing research reviews 4.3 (2005): 422-450.

Henzel, M. Kristi, et al. "Pressure ulcer management and research priorities for patients with spinal cord injury: consensus opinion from SCI QUERI Expert Panel on Pressure Ulcer Research Implementation." J Rehabil Res Dev 48.3 (2011): xi-xxxii.

Theaker, C., et al. "Risk factors for pressure sores in the critically ill."Anaesthesia 55.3 (2000): 221-224

College Answer

Many problems are encountered after hospital discharge. The important problems include Patients have usually had a tracheostomy (and/or prolonged endotracheal intubation) - complications associated with these include laryngeal pathology [eg. polyps, ulcers], aspiration, difficulty with swallowing etc.

°     Limitation of mobility for some time – muscle tone, joint stiffness, Chronic Inflammatory
Polyneuropathy 
°     Skin – hair loss, itching
°     Sexual dysfunction
°     Psychological problems – loss of memory, stress, nightmares, Post Traumatic Stress Disorder, depression, chronic fatigue syndrome
°     Infectious: colonisation with resistant organisms (eg. MRSA)
°     Miscellaneous (loss of taste, loss of appetite, ocular trauma, scarring near region of tape fixing for ETT)
°     Decreased visual acuity in patients who are profoundly hypotensive.
°     Unnecessary medication – Frequently medication commenced in ICU is commenced post discharge.

Tools to asses quality include:

Quality Adjusted Life Years (objective measure),

HAD – Hospital Anxiety & Depression,

SF 36,

PQOL (perceived quality of life),

EuroQOL – European tool
Simpler measures include Glasgow Outcome Scale.

Some hospitals utilise follow up clinics.

Discussion

This question is heavily based on Oh's Manual Chapter 8 (Common  problems  after  ICU).

A systematic response would resemble the following:

• Tracheostomy:
  • Tracheal stenosis
  • Tethering of skin
• Mobility:
  • Muscle wasting, neuromyopathy
  • Slow recovery of normal function (up to 1 year)
• Skin
  • Hair loss
  • Nail ridging
  • MRSA colonisation
  • Facial scraring due to pressure areas from NGT and ETT
• Sexual dysfunction
  • a 39% incidence
• Psychological problems
  • PTSD, in about 15% (27.5% for ARDS survivors)

The question about tools to assess the quality of life is derived from Oh's Manual as well, specifically Box 8.1 on page 62 of the new edition ("Quality of life tool examples").

The contents of this box:

• QALY(Quality Adjusted Life Years - the only objective tool)
• HAD (Hospital Anxiety and Depression)
• PQOL (Percieved Quality of Life)
• EuroQol
• SF 36 (36 item short-form survey)

References

Oh's Intensive Care manual: Chapter 8 (pp.61)  Common  problems  after  ICU   by Carl  S  Waldmann  and  Evelyn  Corner

College Answer

29.1     Define delirium.

A disturbance of consciousness with inattention accompanied by a change in cognition or perceptual disturbance that develops over a short period of time and fluctuates over time. DSM4. Inattention is one of the hallmarks and pivotal features of delirium.

29.2     What is the prevalence of delirium in the critically ill?

Reported as being greater that 8 out of 10 (An answer suggesting that it is highly prevalent should get some credit.

29.3     What is its prognostic significance?

The presence of delirium has been assoc with increased mortality, prolonged ICU and hospital stay, greater dependency on community services and care on discharge and higher nursing home placement rates.

29.4     Briefly outline how you will manage delirium in the critically ill patient.

Treatment of Delirium (marks) – Early recognition
Identify etiology (metabolic, infective, drugs, drug withdrawal,alcohol etc) and treat this

Non Pharmacologic treatment i.e. recurrent orientation of patients, early mobilization, early removal of catheters etc
Pharmacologic- 
Benzodiazepines Thiamine Haloperidol
decrease analgesics sedatives and anticholinergic drugs. NOTE there are NO FDA drugs approved for the treatment of delirium.

Discussion

Delirium is discussed in greater detail elsewhere ("Delirium in the ICU").

It is also covered in some depth in the answer to Question 6 from the second paper of 2013, "Define delirium and describe your management approach to this problem in the ICU. "

However, prevalence and prognostic significance are not discussed in the 2013 paper.

Thus:

Prevalence of delirium in the ICU

"An answer suggesting that it is highly prevalent should get some credit." Indeed, recent publicationsquote a figure of 32-77%.

Prognostic significance of delirium in the ICU

The 2004 Ely prospective cohort study gets brought out whenever anybody talks about the prognostic significance of delirium in the ICU. There are many others. In summary, their findings were as follows:

• Mortality at 6 months: increases × 3.2
• Length of hospital stay doubles
• Every additional day of delirium increases the hazard of deatha t 1 year by about 10%.
• Increased risk of cognitive impairment in the long term (in ~ 70%)

References

Cavallazzi, Rodrigo, Mohamed Saad, and Paul E. Marik. "Delirium in the ICU: an overview." Ann Intensive Care 2.1 (2012): 49.

Ely, E. Wesley, et al. "Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit." Jama 291.14 (2004): 1753-1762.

College Answer

(a)        What does this image show?

A     creamy     supernatant      in     blood     tubes     (serum     and     plasma)     due     to     severe hypertriglyceridaemia (lipaemic serum).

(b)        List three (3) causes for this appearance in blood samples from critically ill patients.

Familial hyperlipedemia
Propofol infusion
TPN use
Pancreatitis  from hyperlipedemia

(c)        If  the  condition  causing  this  appearance  in  the  blood  tubes  were  to  be  long standing, what clinical signs specific to this condition may be found in this patient?

Eyes

• Lipaemia retinalis
• Corneal arcus senilis
• Xanthelasma

Skin

• Xanthomata
• Tendon
• Eruptive

Discussion

Of the ICU trainees, I am sure very few would have seen such a thing as this.

The specific "chicken fat" supernatant demonstrated in the college photograph is characteristic - that "cream" is all chylomicrons. In fact, this finding had in the olden days formed part of the classification of hyperlipidaemias- they used to observe "standing serum" to see if a supernatant would form. In the most severe forms of hyperlipidaemia, this fatty impurity can cause the blood to look milky and turbid.

There is little one can add to the college answer.

References

FREDRICKSON, DONALD S. "An international classification of hyperlipidemias and hyperlipoproteinemias." Annals of internal medicine 75.3 (1971): 471-472.

Aviram, Michael, Yael Sechter, and J. Gerald Brook. "Chylomicron-like particles in severe hypertriglyceridemia." Lipids 20.4 (1985): 211-215.

College Answer

Risk of VTE is high based on:
•  Major trauma with pelvic and lower limb injury and operative intervention
•  Possibility of a pro-thrombotic disorder

Therapy also has potential risks:
•  Risk of intracranial haematoma expansion with unfractionated or LMW heparin

Management options:
•    Quantify      potential      pro-thrombotic     disorder:      ancillary      history,      previous investigations etc
•  Unilateral mechanical prophylaxis
•  Discuss timing of pharmacological prophylaxis
•  Clinical and imaging surveillance
•  IVC filter

Discussion

One can approach this question systematically:

The risk factors for PE are discussed in a separate chapter, but it is a general outline - not specific to ICU patients. The table of undifferentiated risk factors is reproduced below:

Thus, according to these generic risk factors, the patient in the question has several reasons to develop a venous thromboembolism: surgery, trauma, immobility, and a CVC. On top of that, he (a 30 year old man) has already had a DVT at the age of 27, which rings alarm bells. Does he have a weird prothrombotic diathesis? Who knows.

In view of this, he sounds like a candidate for some sort of prophylactic therapy.

If one were to answer this question like an adult, one would produce an answer which resembles the following:

Method of anticoagulation

• Initially, mechanical thromboprophylaxis only (one leg)
• Chemical anticoagulation with unfractionated heparin, after a second CT demonstrates no change in the punctate haemorrhages and the SAH.

Rationale for chemical anticoagulation

• This patient has had surgery, trauma, immobility, and a CVC as risk factors.
• The likelihood of VTE is high.
• Chemical anticoagulation improves survival
• Chemical anticoagulation is more effective than mechanical thromboprophylaxis
• There is currently a contraindication to adequate mechanical thromboprophylaxis (the leg fracture should not have a calf compressor on it)
• Unfractionated heparin is inferior to low molecular weight heparin in the context of ICU thromboprophylaxis, but in this case it would be preferred to LMWH because it can be easily reversed with protamine in case of bleeding.

Advantages

• May improve mortality by decreasing risk of VTE
• Reversible anticoagulation

Disadvantages

• The risk of thrombosis may not be reduced
• The risk of bleeding may increase
• The presence of existing intracranial haemorrhage (and no mention of an ICP measuring device) means catastrophic intracranial bleeding may result.
• Vigilant monitoring of clinical and radiological features of increased intracranial pressure may be required
• Advantages of protection from VTE must be weighed against the risk of intracranial bleeding (it is only day 2 post accident)

Alternatives to chemical anticoagulation

• An IVC filter is an option, but it is not without its various adverse effects.
• Purely mechanical thromboprophylaxis is an option, but would be limited to one leg, and would be less effective.

And what if this patient is coagulopathic from his massive transfusion? Should you anticoagulate him, or is he already "auto-anticoagulated"? Well, it turns out, it doesn't matter what you do, these people clot anway. For some reason, coagulopathic surgical patients seem resistant to the effects of thromboprophylaxis.

Realistically speaking, what is this guy's risk of having a major extension of his traumatic subarachnoid bleed? Generally one must say that we really don't know. It is known, however, that haemorrhagic stroke patients who have an unchanged second CT brain don't tend to suffer from any extension of their bleeding. Small scale studies of traumatic brain injuries complicated by haemorrhage also failed to detect any significant increase in the rate of bleed extension due to routine DVT prophylaxis.

References

Anderson, Frederick A., and Frederick A. Spencer. "Risk factors for venous thromboembolism." Circulation 107.23 suppl 1 (2003): I-9.

Tapson, Victor F., et al. "Venous Thromboembolism Prophylaxis in Acutely Ill Hospitalized Medical PatientsFindings From the International Medical Prevention Registry on Venous Thromboembolism." CHEST Journal 132.3 (2007): 936-945.

Edwards, Meghan, et al. "Venous thromboembolism in coagulopathic surgical intensive care unit patients: is there a benefit from chemical prophylaxis?."Journal of Trauma and Acute Care Surgery 70.6 (2011): 1398-1400.

Lilly, Craig M., et al. "Thrombosis Prophylaxis and Mortality Risk among Critically Ill Adults." CHEST Journal (2014).

Alhazzani, Waleed, et al. "Heparin Thromboprophylaxis in Medical-Surgical Critically Ill Patients: A Systematic Review and Meta-Analysis of Randomized Trials*." Critical care medicine 41.9 (2013): 2088-2098.

Levy, A. S., et al. "Association Between Pharmacologic Thromboprophylaxis and Hemorrhage Progression in Patients With Hemorrhagic Stroke." Stroke45.Suppl 1 (2014): A209-A209.

Farooqui, Ali, et al. "Safety and efficacy of early thromboembolism chemoprophylaxis after intracranial hemorrhage from traumatic brain injury: Clinical article." Journal of neurosurgery 119.6 (2013): 1576-1582.

College Answer

List 2 causes (apart from cardiovascular or respiratory) of cyanosis.

•     Severe methemoglobinemia
•      Sulfhemoglobinemia
•     Hemoglobin mutation
•      Polycythaemia
•     Hypothermia / cold
•     High altitude

Discussion

The college presents us with a long and inventive list.

To this list, one can still add a few (obscure) differentials.

Here we go:

• Methylene blue or indocyanine gree dye injection
• Hemosiderosis
• Excess consumption of colloidal silver
• Chronic massive doses of amiodarone
• Chlorpromazine

And, the causes suggested by the college:

• Severe methemoglobinemia (though the blood in these cases is supposed to be chocolate brown)
• Sulfhemoglobinemia
• Hemoglobin mutation (eg. Haemoglobin Beth Israel, etc)
• Polycythaemia
• Hypothermia
• High altitude

References

Nagel, Ronald L., et al. "Hemoglobin Beth Israel: A mutant causing clinically apparent cyanosis." New England Journal of Medicine 295.3 (1976): 125-130.

Walker, H. Kenneth, et al. "Cyanosis." in Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition (1990).

College Answer

•    Transport by any means involves risk to staff and patients
•    Need   to   be   familiar   with   the   use   of   the   transport   vehicle’s   O2,   suction, communications,and other equipment systems.
•    Reduction  in partial pressure  of oxygen  with altitude,  critically  ill patients  who are already dependent on high FiO2 may be further compromised.
•    Expansion of trapped gases – pneumothoraces, intracranial air from injuries
•    Expansion   of  air  containing   equipment   –  ET  tube,  Sengstaken   tube.  ET  cuff pressures will need to be adjusted
•    IABP difficult to transport
•    Risk of hypothermia
•    As water partial pressure falls, risk of dehydration through resp losses and passive humidification important
•    Auscultation is difficult.
•    The ventilated patient is placed in the Trendelenburg and the reverse Trendelenburg positions during take off and landing respectively. This can impact on perfusion and oxygenation.
•    Potential for pacemaker malfunction due to avionic interference.
•    Staff doing air transport should refrain from compressed gas diving for at least 24 hrs prior to transfer.
•    Physical   problems:   cold,   noise,   lighting,   access   to  patient,   motion   sickness, acceleration injuries (eg head to front of plane to avoid increased ICP on takeoff)

Discussion

This answer would benefit from a systematic approach:

Limitations of the aircraft

• Little space for large equipment (eg. ECMO, IABP)
• Little space for gas reserve (O₂)
• Less equipment available
• Little room for CPR
• Changes in aircraft tilt place the patient in Trendelenberg and reverse Trendelberg positions
• Hypothermia can develop in the cold cabin
• The aircraft is noisy
• The lighting is sub-optimal
• Turbulence can cause injuries to the poorly restrained patient

Dangers of altitude: changes in the behaviour of gases

• ETT cuffs expand
• Gas-filled cavities expand (eg. bowel, pneumothorax, pneumoencephalus)
• Partial pressures of gas mixtures is lower (100% FiO2 at 2100m, the standard "cabin altitude" of commercial aircraft, is only 597mmHg)
• Evacuation by air of those who have bee deep-sea diving is best avoided for about 24 hours- decompression sickness may result.

Dangers of altitude: changes in fluid behaviour

• Decreased boiling point at altitude increases the rate of evaporative loss

Dangers of aircraft operation

• Avionics may interfere with pacemakers
• Noise may interfere with equipment alarms
• Vibration interferes with examination of the pulse
• Auscultation is practically impossible
• Motion sickness may cause vomiting and aspiration (it would suck to be intubated purely because of motion sickness)

References

Parsons, Chris J., and Walter P. Bobechko. "Aeromedical transport: its hidden problems." Canadian Medical Association Journal 126.3 (1982): 237.

ANZCA "Guidelines for Transport of Critically Ill Patients

CICM "Minimum Standards for Transport of Critically Ill Patients" (IC-10, 2010)

"Commercial Airliner Environmental Control System: Engineering Aspects of Cabin Air Quality".

College Answer

a) What is this skin rash?
•    Erythema multiforme

b) Give three causes
•    Herpes simplex infection
•    Mycoplasma pneumonia
•    Streptococcal infections
•     Drugs
•     SLE
•     Leukaemia

c) Apart from the skin, what other tissues are involved?
•    Mucous membranes, especially oral mucosa

Discussion

That is a nice shot of erythema multiforme from Wikipedia.

How does one recognise it? Apparently, the lesions are typical. This is a disease of the skin and mucous membranes.

Approximately 50% of cases are associated with herpes simplex.

The rest of the causes can be classified as either infectious or drug-related:

Infectious causes:

• Mycoplasma pneumoniae
• Fungal infections eg. candida

Drugs which cause erythema multiforme:

• Phenytoin
• Barbiturates
• NSAIDs
• Penicillins
• Phenothiazines
• Sulfonamides

References

Clark Huff, J., William L. Weston, and Marciih G. Tonnesen. "Erythema multiforme: a critical review of characteristics, diagnostic criteria, and causes."Journal of the American Academy of Dermatology 8.6 (1983): 763-775.

Leaute-Labreze, C., et al. "Diagnosis, classification, and management of erythema multiforme and Stevens–Johnson syndrome." Archives of disease in childhood 83.4 (2000): 347-352.

College Answer

• Factors predictive of poor outcome:
  • Severe TBI in an elderly patient
  • SDH increased risk of poor outcome
  • Warfarin therapy
  • Pre-existing co-morbidities – renal disease, diabetes, neurological dysfunction

Age-related changes:

• Cardiovascular
  • Increased incidence of coronary artery disease
  • Systolic and diastolic dysfunction with CCF
  • Conduction disorders (SSS, AF, BBB)
  • Valvular disease
  • Decreased response to sympathetic stimulation
• Respiratory
  • Decreased respiratory muscle strength
  • Decreased respiratory centre sensitivity to hypoxia and hypercarbia
  • Reduced elastic recoil of lung
  • Increased chest wall stiffness
  • Reduced vital capacity and FEV1.

Response to medications

• Age has been shown in multiple studies to be an independent risk factor for adverse drug reactions.
• Age related physiological changes affect absorption, distribution, metabolism and elimination of drugs.
• Poly-pharmacy is common, thus increased risk of adverse drug reaction.
• Cognitive impairment and drug errors – overdose, non-adherence, failure to disclose full medication list to often multiple medical practitioners involved in care.
• Reducing renal blood flow and GFR with age alters drug elimination potentially leading to drug accumulation.

Discussion

A more detailed all-systems look at age-related changes in the response to critical illness can be found in Question 8 from the second paper of 2007:"What are the age related factors which adversely affect outcome in the elderly (>65 years) critically ill patient?"

How did the college arrive at this answer?

What are the predictors of poor outcome in traumatic brain injury?

• Everyone seems to agree that age is a predictor of poor outcome.
•  Steyerberg et al found that age was associated with poor neurological outcomes and decreased survical. 
• Amacher et al also found that it doesnt matter how good your GCS is on admission, your old age will still play a role.
• Being over 60 is a poor prognostic indicator.
• Steyerberg et al found that a traumatic subarachnoid (rather than subdural) was a determinant of poor prognosis.
• Mortality in elderly patients with subdural haematoma is very high if they present with a GCS 3-5
• For these people,  craniotomy may not be justified, because of the extremely poor outcomes overall.

As far as age-related physiological changes go...

From this article on geriatric cardiology, I quote the following physiological changes associated with age:

Cardiovascular changes

• A decrease in elasticity and an increase in stiffness of the arterial system. Thus:
  • Increased afterload on the left ventricle
  • left ventricular hypertroph
  • Increase in systolic blood pressurey,
  • Changes in the left ventricular wall that prolong relaxation of the left ventricle in diastole; thus diastolic dysfunction and the propensity towards pulmonary oedema
  • Aortic valve calcification
• Dropout of atrial pacemaker cells resulting in a decrease in intrinsic heart rate.
• With fibrosis of the cardiac skeleton there is calcification at the base of the aortic valve and damage to the His bundle as it perforates the right fibrous trigone.
• Decreased responsiveness to β-adrenergic receptor stimulation
• Decreased reactivity to baroreceptors and chemoreceptors,
• Increase in the levels of circulating catecholamines.

Respiratory changes

• Decrease in exchange surface area ("senile emphysema"):
  • Dilatation of alveoli
  • Enlargement of airspaces
  • loss of supporting tissue for peripheral airways
  • Carbon monoxide transfer decreases with age, reflecting mainly a loss of surface area.
• Decreased static elastic recoil of the lung, thus
  • Increased residual volume
  • Increased functional residual capacity.
• Decreased expiratory flow rates (especially small airways)
  • The ventilation/perfusion ratio heterogeneity increases, with low V/Q zones appearing as a result of premature closing of dependent airways.
• Decreased compliance of the chest wall, thus increased work of breathing
• Decreased respiratory muscle strength (though this depends on the heart, and on nutrition)
• Decreased sensitivity of respiratory centres to hypoxia and hypercapnia

Pharmacokinetic changes:

• Reduction in first-pass metabolism, thus increased oral bioavailability of a few drugs.
• Body fat increases, body water decreases; thus:
  • Hydrophilic drugs have a smaller volume of distribution
  • lipophilic drugs have an increased volume of distribution and a longer half-life
• Drugs with a high hepatic extraction ratio decrease in systemic clearance
• Activities of cytochrome P450 enzymes are preserved in normal ageing
• Renal clearance may be decreased due to age-related changes in renal function

References

Langlois, Jean A., Wesley Rutland-Brown, and Marlena M. Wald. "The epidemiology and impact of traumatic brain injury: a brief overview." The Journal of head trauma rehabilitation 21.5 (2006): 375-378.

Steyerberg, Ewout W., et al. "Predicting outcome after traumatic brain injury: development and international validation of prognostic scores based on admission characteristics." PLoS medicine 5.8 (2008): e165.

Stocchetti, Nino, et al. "Traumatic brain injury in an aging population." Journal of neurotrauma 29.6 (2012): 1119-1125.

Amacher, Loren A., and David E. Bybee. "Toleration of head injury by the elderly." Neurosurgery 20.6 (1987): 954-958.

Jamjoom, Abdulhakim, et al. "Outcome following surgical evacuation of traumatic intracranial haematomas in the elderly." British journal of neurosurgery 6.1 (1992): 27-32.

Cheitlin, Melvin D. "Cardiovascular physiology—changes with aging." The American journal of geriatric cardiology 12.1 (2003): 9-13.

Shi, Shaojun, and Ulrich Klotz. "Age-related changes in pharmacokinetics."Current drug metabolism 12.7 (2011): 601-610.

Corsonello, A., C. Pedone, and R. Antonelli Incalzi. "Age-related pharmacokinetic and pharmacodynamic changes and related risk of adverse drug reactions." Current medicinal chemistry 17.6 (2010): 571-584.

Carbonin, P., et al. "Is age an independent risk factor of adverse drug reactions in hospitalized medical patients?." Journal of the American Geriatrics Society39.11 (1991): 1093-1099.

Timiras, Paola S., ed. Physiological basis of aging and geriatrics. CRC Press, 2013.

Janssens, J. P., J. C. Pache, and L. P. Nicod. "Physiological changes in respiratory function associated with ageing." European Respiratory Journal 13.1 (1999): 197-205.

College Answer

a)

i. Abnormal features and diagnosis:

Tight, indurated skin with limited mouth opening and beak-like facies Telangiectasia

Scleroderma (or CREST syndrome if other features are present)

ii. Management problems:

• • Difficult intubation
  • Aspiration risk
  • Risk of oesophageal perforation with instrumentation
  • Limited respiratory reserve
  • Pulmonary hypertension
  • Difficulty palpating peripheral pulses
  • Difficult vascular access and risk of digital gangrene with arterial lines and vasopressors
  • Increased risk of renal failure
  • Immunosuppression
  • Malabsorption and nutritional deficiencies
  • Skin breakdown / pressure areas

b)

• Clinical features of acute bowel ischaemia:
  • •   Abdominal pain
  • •   Abdominal tenderness
  • •   Shock
  • •   Bloody diarrhoea or haematochezia
  • •   Evidence of ileus (vomiting, large NG aspirates, feed intolerance)
  • •   Absent/reduced bowel sounds

• Briefly describe the distribution of the arterial blood supply to the large and small bowel.

• • •   Extensive collateral circulation
  • •   Coeliac axis supplies the gut down to the opening of the bile duct (mid duodenum).
  • SMA supplies the bowel from the entrance of the bile duct (mid duodenum) to a level just short of the splenic flexure of the colon. (to splenic flexure or right two thirds of the transverse colon acceptable)
  • IMA supplies the bowel from just short of the splenic flexure of the colon, to the rectum and anus. The rectum and anus also receive blood via branches of the internal iliac artery.

Discussion

More stolen images; though I expect the watermarks identify them well. The face is from dermis.net, and represents scleroderma. The hands are from the Rheumatology Image Bank; the digits demonstrate features of acrosclerosis, contracture and terminal phalangeal resorption.

Issues with these patients can be discussed in a systematic manner:

1.  Difficult intubation:
   1. Limited neck extension
   2. Limited mouth opening
2.   Respiratory involvement:
   1. Pulmonary fibrosis
   2. Restrictive lung disease
   3. Pulmonary hypertension
   4. SpO₂ monitoring may be frustrated by poor end-digital perfusion
   5. The rapidly fatal "scleroderma-pulmonary-renal syndrome (SPRS)" may develop, which manifests as a fulminant course of acute normotensive renal failure associated with diffuse alveolar hemorrhage.
3. Cardiovascular involvement of the disease process:
   1. Cardiac problems:
      1. Arrhythmias,
      2. Myocardial fibrosis (thus, restrictive diastolic failure)
      3. Pericardial stricture (also restricts diastolic filling)
   2. Vascular problems
      1. Difficult vascular access: the skin, being very thick, makes it difficult to palpate vessels (veins and arteries both)
      2. Poor distal perfusion of the extremities, leading to gangrene- as one might expect this is not improved by arterial cannulation.
      3. Poor skin perfusion promotes pressure areas
4. Neurological sequelae: 
   1. Corticosteroid-associated psychosis
   2. Cerebral vasculitis
5. Electrolyte disturbances
   1. Hyponatremia and fluid retention due to corticosteroid therapy
   2. Hyperkalemia due to renal failure
6. Renal involvement
   1. Renal failure, renal artery stenosis
   2. Scleroderma "renal crisis"
7. Gastrointestinal and nutritional issues
   1. Oesophagitis
   2. Poor gut motility
   3. Decreased feed tolerance
   4. Risk of aspiration.
   5. Risk of oesophageal perforation
   6. Telangiectasia is present also on mucosal surfaces; there is an increased risk of bleeding from upper GI sites
8. Haematological problems:
   1. Anaemia of chronic disease is coupled with the poor EPO synthesis from damaged kidneys.
   2. Bone marrow function may be suppressed in other ways, particularly if serious immunosuppresants are in use (eg. cyclophosphamide)
9.     Immunosuppressive therapy
   1. Increased infection risk

Clinical features of acute bowel ischaemia:

• Abdominal pain, out of proportion to the signs
• Peritonism
• Abdominal distension
• Absent bowel sounds
• Ileus
• Bloody stool
• Metabolic acidosis
• Hemodynamic instability

Blood supply to the bowel

This is easy anatomy to remember; there are only two arteries.

Main points:

• Extensive collateral supply
• Coeliac axis: up to duodenum
• SMA: duodenum to splenic flexure
• IMA: splenic flexure to anus.

References

Farber, Harrison W., Robert W. Simms, and Robert Lafyatis. "Analytic Review: Care of Patients With Scleroderma in the Intensive Care Setting." Journal of intensive care medicine 25.5 (2010): 247-258.

Legerton 3rd, C. W., Edwin A. Smith, and Richard M. Silver. "Systemic sclerosis (scleroderma). Clinical management of its major complications."Rheumatic diseases clinics of North America 21.1 (1995): 203-216.

Oldenburg, W. Andrew, et al. "Acute mesenteric ischemia: a clinical review."Archives of internal medicine 164.10 (2004): 1054-1062.

Thorek, Philip. "Blood Supply of the Gut." Anatomy in Surgery. Springer New York, 1985. 558-562.

College Answer

Mode of transfer – road or air (fixed or rotary wing) – should be determined by resources, distance to be covered and weather conditions. The mode of transfer should provide the shortest time from the referring hospital to the receiving centre and the standard of care should be maintained throughout the transfer. Staff safety during transfer is an essential consideration. College guidelines for minimum standards for transport of critically ill patients should be followed.

Co-ordination and communication

Ensure bed available at receiving centre

Establish key individual(s) at receiving centre for liaison to receive updates on transfer status and to provide expert advice re patient management

Ensure all necessary documentation prepared to accompany patient including clinical records and radiology 
Ensure transport team know destination (town, hospital, ICU location)

Ensure patient’s next of kin are aware of need for transfer

Preparation of patient

Consider intubation and mechanical ventilation (with ongoing sedation and paralysis) depending on stability of patient and distance/mode of transport

Stabilise on transport ventilator

Vascular access including arterial line

Urinary catheterization and passage of NG tube TEDs

All lines and tubes secured and correct position confirmed Resuscitation and physiological stabilization of patient as indicated Final repeat clinical assessment immediately prior to departure

Monitoring 
Full monitoring of patient including intra-arterial pressure, end-tidal CO2, oxygen saturation and ECG and TO4 if paralysing agents used

Ensure optimum MAP to maintain cerebral perfusion but target SBP < 150 mmHg to avoid re-bleed

Equipment and drugs

• Transport ventilator 
• Monitor
• Bag-valve-mask and re-intubation equipment 
• Oxygen cylinders 
• Defibrillator
• Infusion pumps as needed 
• Needles and syringes etc
• Sedative drugs and muscle relaxants 
• Resuscitation drugs
• IV fluids 
• Prescribed drugs as indicated eg antibiotics

Personnel

Ensure adequately trained personnel for retrieval team, including appropriately experienced medical practitioner

Ensure adequate staffing remains on site at base hospital

Discussion

These retrieval questions should be approached with some sort of a system. ANZCA also have a policy document- Guidelines for Transport of Critically Ill Patients- which has been endorsed by CICM.

CICM have a policy document - Minimum Standards for Transport of Critically Ill Patients (IC-10, 2010) which is referred to in the college answer. This document provides a reasonable systematic framework. It is, however, a 12-page document.

In an abridged form, the recommendations are as follows:

Vehicle

• Determined by nature of illness and urgency or retrieval
• Need to be mindful of the effects of transport on the illness (eg. the effect of low cabin pressure on gas-filled obstructed bowel loops)
• Number of staff and volume of equipment
• Road conditions, weather conditions

Equipment

• Airway equipment
• Pericardiocentesis equipment
• Pleural drainage eqipment
• Suction
• Ventilator
• Oxygen supply (in excess)
• Defibrillator
• Thermal insulation
• Monitoring equipment
• All drugs checked and labelled

Monitoring

• Pulse oximeter
• Capnometer
• ECG
• NIBP or arterial line
• Airway equipment must have disconnection alarms

Patient preparation

• Ideal patient is intubated, ventilated and paralysed
• The patient should ideally be stabilised on a transport ventilator before departure
• Vascular access should be secure; you should not be doing any elective procedures during transfer
• One last pre-departure assessment

Communication:

• Bed availability
• Accepting primary consultant
• Accepting unit (ICU)
• Next of kin
• Documentation travels with the patient

References

ANZCA "Guidelines for Transport of Critically Ill Patients

CICM "Minimum Standards for Transport of Critically Ill Patients" (IC-10, 2010)

College Answer

a)

• Severe drug hypersensitivity reaction
• Erythema multiforme 
• Stevens Johnson/TENS
• Viral infection 
• Herpes simplex
• Varicella 
• EBV/CMV
• Bacterial infection – staphylococcal scalded skin syndrome 
• Autoimmune bullous disease
• Urticarial vasculitis

b)

• Skin biopsy 
• HSV and varicella PCR
• Viral serology 
• Mycoplasma serology

Discussion

The college did not provide us with a picture of the patient. Given the breadth of differential diagnosis offered, it is difficult to Google a satisfactory rash picture for this question. The picture of the back is a shot of somebody with Stevens-Johnson syndrome, stolen from Medscape; the face is apparently also SJS but it is from the slightly less reputable studyblue.com, where it is featured as a flashcard.

Without reliable pictures from the college paper, it is difficult to generate a sensible list of counter-differentials to match the college answer.

However, at this stage the author of these notes must humbly confess that even if the rash picture was available in high resolution, he would likely still be powerless against its mysteries.

In view of this, here is a generic list of differentials one could spout, for the question "name that rash". It is so generic that it is applicable even if one cannot see the skin.

Vascular causes:

• Shower of emboli
• Vascular insufficiency

Infectious causes:

• Toxic epidermal necrolysis
• Staphylococcal scalded skin syndrome
• Viral exanthem/manifestations of viral infection
• Fungal infection eg. candida
• Streptococcal toxic shock syndrome (erythroderma)

Neoplastic causes:

• Cutaneous lymphoma/leukaemia

Drug-related causes

• Stevens Johnson syndrome
• Red Man syndrome (vancomycin)

Autimmune cause

• Allergic reaction
• Vasculitis
• Erythema multiforme
• Graft-versus-host disease
• Bullous pemphigoid

Traumatic causes

• Burns

The standard work-up:

• FBC for eosinophilia
• Viral serology for HSV, VZV, HIV, EBC, CMV
• Culture of exudate
• Mycoplasma serology
• Vasculitic screen
• Skin biopsy

References

Ely, John W., and Mary Seabury Stone. "The generalized rash: Part I. Differential diagnosis." Am Fam Physician 81.6 (2010): 726-734.

Bachot, Nicolas, and Jean-Claude Roujeau. "Differential diagnosis of severe cutaneous drug eruptions." American journal of clinical dermatology 4.8 (2003): 561-572.

College Answer

Therapeutic or diagnostic

Therapeutic:

CT or US guided drainage of abscess or fluid collections

Coiling of aneurysm

Embolisation of bleeding vessel Regional thrombolysis or clot removal TIPS procedure

Angioplasty for vasospasm Coronary intervention 
IVC filter insertion

Angioseal of cannulated vessel eg inadvertent arterial insertion of vascath Vascular access eg Hickman

Insertion PEG, nasojejunal tubes

Diagnostic:

Angiography to diagnose vasculitis, cerebral thrombosis, region of haemorrhage (especially intestinal), brain death

Efficacy

May be as effective as surgery (good evidence in aneurysmal SAH) with lower morbidity and mortality

Offers treatment option for patients unsuitable for surgery due to age or co-morbidities Good option in critically ill where surgical risks high eg laparotomy to drain abscess Preferred strategy in management pelvic trauma 
May avoid hysterectomy in post-partum haemorrhage

Limitations

Specific expertise needed but increasingly widespread

Needs to be performed in radiology suite with the risks and difficulties of managing a critically ill patient in a ‘hostile’ environment

Surgical back-up needed if intervention fails Risk of contrast use (allergy, CIN) Complications specific for each procedure

Discussion

These "discuss the role" questions are difficult to answer in a systematic fashion. The college suggests we "explain the underlying key principles".

The provided answer divides the issue into therapeutic and diagnostic roles, and then discusses the limitations of interventional radiology as a whole. This sort of structure lends itself well to a tabulated format.

References

Harris, K. G., et al. "Diagnosing intracranial vasculitis: the roles of MR and angiography." American journal of neuroradiology 15.2 (1994): 317-330.

Hunnam, G. R., and C. D. R. Flower. "Radiologically-guided percutaneous catheter drainage of empyemas." Clinical radiology 39.2 (1988): 121-126.

Nicolaou, Savvas, et al. "Ultrasound-guided interventional radiology in critical care." Critical care medicine 35.5 (2007): S186-S197.

College Answer

Introduction / Rationale

A daily interruption of sedation is a strategy designed to reduce exposure to sedative agents, allow assessment of neurological status and assess readiness for extubation and to reduce duration of mechanical ventilation.

Evidence

Initial trials showed a marked reduction in duration of mechanical ventilation, and decreased duration of intensive care length of stay (e.g. Kress et al, NEJM 2000). It was notable that no sedation target nor protocol was used in the control group, thus this group may have been oversedated, analogous to the 12ml/kg TV group in the ARDSNET low TV trial.

Subsequent studies have been somewhat conflicting:

• ABC study (Girard et al, Lancet 2008) showed improved outcomes (mortality, less time on mechanical ventilation, reduced ICU length of stay) in patients treated with a paired daily interruption of sedation and a spontaneous breathing trial compared to usual care plus a spontaneous breathing trial.
• SLEAP study (Mehta et al JAMA, 2012) showed no difference in outcomes comparing protocolised sedation to protocolised sedation plus daily interruption of sedation.

Disadvantages / Adverse effects / Limitations

Potential adverse effects of daily interruption of sedation:

• Patient discomfort and risk of PTSD and other long term psychological issues
• Dislodgment of ETT, CVC, arterial lines etc.
• Increased nursing workload.
• Cessation of sedation could lead to agitation which can be associated with physiological instability, hypertension, tachycardia, ventilator dysynchrony and hypoxaemia, which could be associated with exacerbation of primary disease in certain conditions, e.g. myocardial ischaemia, brain injury.
• I.e. interruption of sedation contra-indicated in above patient groups.

Own Practice

Any reasonable justifiable approach acceptable.

Summary

Daily interruption of sedation may have a role in physiologically stable patients in ICUs that do not routinely use protocolised sedation.

Discussion

Rationale

• Exposure to sedating agents is undesirable, given that most agents have unpleasant side-effects
• Interruptions in sedation may decrease the total dose of sedation over the course of one's ICU stay

Proposed advantages

• More rapid weaning from ventilation
• Reduction in ICU length of stay
• Reduced need for vasopressors
• Reduced need for fluid boluses

Expected disadvantages

• Greater risk of self-extubation
• Greater psychological distress; potential for PTSD
• Increased nursing workload
• Increased patient-ventilator dyssynchrony

Evidence:

• Kress et al (2000) - small single centre RCT; n=128
  • length of stay in ICU and duration of ventilation was reduced
• Kress et al (2003) - small single centre RCT; n=108
  • reduced symptoms of PTSD; no adverse psychological outcome
• Girard et al (2008) - multicentre trial, n=336
  • Reduced mortality at 1 year, but increased risk of self-extubation
• Mehta et al (2012) - multicentre randomised controlled trial, n=430
  • No reduction in length of ICU stay or duration of ventilation
• Cochrane verdict (2014) - meta-analysis, n=1282; no strong evidence in support of this practice. Tracheostomy may be performed less often.

References

Kress, John P., et al. "Daily interruption of sedative infusions in critically ill patients undergoing mechanical ventilation." New England Journal of Medicine342.20 (2000): 1471-1477.

Kress, John P., et al. "The long-term psychological effects of daily sedative interruption on critically ill patients." American journal of respiratory and critical care medicine 168.12 (2003): 1457-1461.

Girard, Timothy D., et al. "Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomised controlled trial." The Lancet 371.9607 (2008): 126-134.

Mehta, Sangeeta, et al. "Daily sedation interruption in mechanically ventilated critically ill patients cared for with a sedation protocol: a randomized controlled trial." JAMA 308.19 (2012): 1985-1992.

Burry, L., et al. "Daily sedation interruption versus no daily sedation interruption for critically ill adult patients requiring invasive mechanical ventilation." The Cochrane Library 2014, Issue 7

College Answer

Definition:

The acute onset of a disturbance of consciousness with inattention, changes in cognition and/orperception, that fluctuates over time, occurs as a consequence of a general medical condition and isnot better accounted for by a pre-existing, established or evolving dementia.

Management:

1. Early recognition of delirium.

2. Stabilise and ensure safety of the patient:

• • Attend to airway, breathing and circulation issues as required.

3. Consider and rule out any potentially life-threatening causes of delirium (comprehensive history and physical examination will provide clues):

• • Hypoxia
  • Hypoglycaemia
  • Intra-cerebral haemorrhage
  • Meningitis/Encephalitis
  • Poisoning
  • Wernicke’s Encephalopathy
  • Infection: local (wound, anastomotic leaks etc.), UTI, lung etc.
  • Withdrawal from drugs
  • Hypertensive encephalopathy
  • Metabolic derangements – sodium, renal, liver.

4. Consider non-pharmacological strategies to control symptoms:

• • Application of hearing aids, spectacles and dentures if worn.
  • Continuous re-orientation of patient - verbal, visual with photographs etc.
  • Enlist help of family members and/or interpreters.

• • Ensure as close to normal as possible sleep/wake cycles in a quiet and calm environment.
  • Treat pain, constipation, urinary retention if present.

• • Check drug chart and beware/attend to poly-pharmacy and cessation of drugs associated with delirium.
  • Mobilise early.
  • Avoid physical restraints if safe to do so.

5. Obtain pharmacological control of symptoms if necessary:

• • Anti-psychotics are first line agents e.g. haloperidol, olanzepine, quetiapine.

• • Haloperidol 1-5mg iv q30 PRN. Dose can be doubled and repeated. Beware long QTc.

• • Benzodiazepines as first line agents for alcohol withdrawal only. Often used in combination with anti-psychotics in difficult to control symptoms in non-alcohol withdrawal delirium.

6. Treat cause if found:
7. O2, antibiotics, thiamine, glucose, electrolyte replacement, intra-venous fluids if dehydrated.

13

Investigations:

Directed by history, physical examination and differential diagnosis but include/consider;

Basic:

FBC, EUC, Glucose, LFT, ABG, CXR, ECG, Urinalysis + Dipstick, Septic screen, Urinary Drug Screen.

Advanced:

CT Brain, LP, TTE.

Discussion

Delirium is a favourite of the examiners. It is discussed in greater depth elsewhere ("Delirium in the ICU")

In order to simplify revision, I reproduce the salient points here:

A systematic approach to this question would resemble the following:

Urgently exclude and manage any lifethreatening aetiologies of delirium:

A) - Look for airway compromise due to decreased level of consciousness

B) - Assess for hypoxia and hypercapnea

C) - Assess for hypotension (thus cortial hypoperfusion) or hypertension (thus, hypertensive encephalopathy)

D) - Exclude hypoglycaemia and intoxication or poisoning; investigate for focal intracranial causes of delirium, such as intracranial haemorrhage or space-occupying lesion. Think about non-convulsive status epilepticus as the cause of delirium. Also consider withdrawal from alcohol and other drugs.

E) - Evaluate electrolytess, looking for hyponatremia

F) - Assess renal function, looking for uremia and dehydration

G) - Assess hepatic function, suspecting hepatic encephalopathy. Don't forget Wernicke's.

H) - Assess bone marrow function - cytopenia may be a clue to a space-occupying metastatic lesion, whereas blood film findings such as macrocytosis may suggest a chronic nutritional deficiency associated with alcoholism or IV drug abuse.

I) - Assess temperature, inflammatory markers and features of sepsis, ranging from UTI to septic shock (thinking about septic encephalopathy). Consider neurosyphilis and think about meningitis or encephalitis.

Investigation of delirium:

Stemming from the abovementioned differentials,

• ABG
• Urinalysis
• EUC
• CMP
• FBC
• Blood film
• Inflammatory markers
• CT brain
• EEG
• Lumbar puncture

Management of delirium

Non-pharmacological:

• • Good analgesia
  • Clear and firm communication with the patient
  • Frequent re-orientation
  • Family presence
  • Low-noise environment
  • Restoration of hearing aids and spectacles
  • Avoidance of sleep disturbance, promotion of normal sleep–wake cycle.
  • Avoidance of physical restraints
  • Early removal of IV lines and IDCs

Pharmacological:

• • Dexmedetomidine
  • Atypical antipsychotics
  • Classical antipsychotics
  • Benzodiazepines (if withdrawing from alcohol or benzodiazepines)

References

Oh's Intensive Care manual: Chapter 49   (pp. 549) Disorders  of  consciousness  by Balasubramanian  Venkatesh

Girard, Timothy D., Pratik P. Pandharipande, and E. Wesley Ely. "Delirium in the intensive care unit." Critical Care 12.Suppl 3 (2008): S3.

Ely, E. Wesley, et al. "Evaluation of delirium in critically ill patients: validation of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU)."Critical care medicine 29.7 (2001): 1370-1379.

O'Keeffe, SHAUN T., and JOHN N. Lavan. "Clinical significance of delirium subtypes in older people." Age and ageing 28.2 (1999): 115-119.

Barr, Juliana, et al. "Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit." Critical care medicine 41.1 (2013): 263-306.

Ouimet, Sébastien, et al. "Incidence, risk factors and consequences of ICU delirium." Intensive care medicine 33.1 (2007): 66-73.

Girard, Timothy D., et al. "Delirium as a predictor of long-term cognitive impairment in survivors of critical illness." Critical care medicine 38.7 (2010): 1513.

Hopkins, Ramona O., and James C. Jackson. "Long-term neurocognitive function after critical illness." CHEST Journal 130.3 (2006): 869-878.

van den Boogaard, Mark, et al. "Incidence and short-term consequences of delirium in critically ill patients: a prospective observational cohort study."International journal of nursing studies 49.7 (2012): 775-783.

Stevens, Robert D., Karin J. Neufeld, and Tarek Sharshar. "Delirium in the ICU: time to probe the hard questions." Crit Care 15.1 (2011): 118.

van Boogaard, M., et al. "Development and validation of PRE-DELIRIC (PREdiction of DELIRium in ICu patients) delirium prediction model for intensive care patients: observational multicentre study." BMJ: British Medical Journal344 (2012).

Van Rompaey, Bart, et al. "Risk factors for intensive care delirium: a systematic review." Intensive and Critical Care Nursing 24.2 (2008): 98-107.

Schweickert, William D., et al. "Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomised controlled trial."Lancet (London, England) 373.9678 (2009): 1874-1882.

Skrobik, YoannaK, et al. "Olanzapine vs haloperidol: treating delirium in a critical care setting." Intensive care medicine 30.3 (2004): 444-449.

Milbrandt, Eric B., et al. "Haloperidol use is associated with lower hospital mortality in mechanically ventilated patients*." Critical care medicine 33.1 (2005): 226-229.

Moots, R. J., et al. "Old drug, new tricks: haloperidol inhibits secretion of proinflammatory cytokines." Annals of the rheumatic diseases 58.9 (1999): 585-587.

Page, Valerie J., et al. "Effect of intravenous haloperidol on the duration of delirium and coma in critically ill patients (Hope-ICU): a randomised, double-blind, placebo-controlled trial." The Lancet Respiratory Medicine 1.7 (2013): 515-523.

Gilchrist, Neil A., Ifeoma Asoh, and Bruce Greenberg. "Atypical antipsychotics for the treatment of ICU delirium." Journal of intensive care medicine 27.6 (2012): 354-361.

Jasiak, Karalea D., et al. "Evaluation of discontinuation of atypical antipsychotics prescribed for ICU delirium." Journal of pharmacy practice 26.3 (2013): 253-256.

Inouye, Sharon K., et al. "A multicomponent intervention to prevent delirium in hospitalized older patients." New England journal of medicine 340.9 (1999): 669-676.

Girard, Timothy D., et al. "Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomised controlled trial." The Lancet 371.9607 (2008): 126-134.

Mehta, Sangeeta, et al. "Daily sedation interruption in mechanically ventilated critically ill patients cared for with a sedation protocol: a randomized controlled trial." JAMA 308.19 (2012): 1985-1992.

Devlin, John W., et al. "Efficacy and safety of quetiapine in critically ill patients with delirium: A prospective, multicenter, randomized, double-blind, placebo-controlled pilot study*." Critical care medicine 38.2 (2010): 419-427.

Kim, Sung‐Wan, et al. "Risperidone versus olanzapine for the treatment of delirium." Human Psychopharmacology: Clinical and Experimental 25.4 (2010): 298-302.

Grover, Sandeep, Vineet Kumar, and Subho Chakrabarti. "Comparative efficacy study of haloperidol, olanzapine and risperidone in delirium." Journal of psychosomatic research 71.4 (2011): 277-281.

Yoon, Hyung-Jun, et al. "Efficacy and safety of haloperidol versus atypical antipsychotic medications in the treatment of delirium." BMC psychiatry 13.1 (2013): 1-11.

College Answer

• a) Rheumatoid arthritis.

• b) Ulnar deviation:
  • Z deformity of the thumb
  • Boutonnieres deformity (left little finger)
  • Swan neck deformity (right middle and ring fingers)
  • Swelling of metacarpo-phalangeal joints
  • Wasting of small muscles of the hand

• c) Pleural effusion:
  • Pleural thickening.
  • Nodules.
  • Interstitial fibrosis.
  • Bronchiectasis.
  • Skeletal rheumatoid changes e.g. shoulder arthritis.
  • Caplan’s syndrome in patients with pneumoconiosis.

20

Discussion

The free-to-use image displayed above is not the image from the CICM paper, but a picture of rheumatoid arthritis hands from a Wikipedia article.

The following physical signs are still obvious:

• Ulnar deviation
• Z deformity of the thumb
• Swan neck deformities (middle image)
• Swelling of metacarpo-phalangeal joints
• Wasting of small muscles of the hand (right image)
• Boutonnieres deformity is not obvious, but is probably present in the right image

In general, the clinical features of rheumatoid arthritis include the following:

• Symmetric joint swelling, MCP > DIP
• Morning stiffness  lasting at least 1 h before maximal improvement 
• Extra-articular synovitis (tenosynovitis, bursitis)
• General symptoms (malaise, fatigue, weight loss, fever)
• Hand signs as mentioned above:
  • Ulnar deviation
  • Z deformity of the thumb
  • Swan neck deformities
  • Swelling of metacarpo-phalangeal joints
  • Wasting of small muscles of the hand
  • Boutonnieres deformity

The site clinicalexam.com has an excellent entry on RA, with extensive lists of signs and examination techniques.

Pulmonary involvement in rheumatoid arthritis tends to manifest in the following ways:

• Pleurisy/pleural effusion 
• Pneumothorax 
• Rheumatoid nodulosis 
• Interstitial pulmonary fibrosis
• Caplan's syndrome is the combination of rheumatoid nodules and pneumoconiosis
• Bronchiectasis
• Pulmonary vasculitis
• Methotrexate-induced interstitial pulmonary fibrosis

References

​Talley and O'Connor is a good source for the clinical features of RA.

Arnett, Frank C., et al. "The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis." Arthritis & Rheumatism31.3 (1988): 315-324.

Anaya, Juan-Manuel, et al. "Pulmonary involvement in rheumatoid arthritis."Seminars in arthritis and rheumatism. Vol. 24. No. 4. WB Saunders, 1995.

Grassi, Walter, et al. "The clinical features of rheumatoid arthritis." European Journal of Radiology 27 (1998): S18-S24.

Krane, S. M., and L. S. Simon. "Rheumatoid arthritis: clinical features and pathogenetic mechanisms." The Medical clinics of North America 70.2 (1986): 263-284.

College Answer

Physiotherapists are part of the multidisciplinary team providing care to patients in the ICU.

Physiotherapists perform an assessment that includes the respiratory, cardiovascular, neurological, and musculoskeletal systems to formulate treatment plans.

The traditional focus of treatment has been the respiratory management of both intubated and spontaneously breathing patients however emerging evidence of the longstanding physical impairment suffered by survivors of intensive care has resulted in physiotherapists re-evaluating treatment priorities to include exercise rehabilitation as a part of standard clinical practice.

The goals of respiratory physiotherapy management are to promote secretion clearance, and to maintain or recruit lung volume, in both the intubated and spontaneously breathing patient. In the intubated patient, physiotherapists commonly employ manual and ventilator hyperinflation and positioning as treatment techniques whilst in the spontaneously breathing patients there is an emphasis on mobilisation.

Physiotherapists have a role in maintaining joint and muscle function in those who are at risk of contractures, for example in neurological injuries and patients with prolonged paralysis. A trend toward an emphasis on exercise rehabilitation over respiratory management is increasingly evident as survivors of a prolonged ICU stay can suffer deconditioning, muscle atrophy, and weakness that may impact upon quality of life.

Additional roles include the fitting of cervical collars, spinal braces, slings etc. in trauma patients, setting up TENS machines and patient education (exercise, rehab etc.)

Discussion

This topic merited an entire chapter in Oh's Manual; and therefore we can expect that this question is the college's way of investigating whether or not anybody has read that chapter. Specifically, the chapter begins with a list of the main roles of the physiotherapist in the ICU.

Thus, it is the primary source for the answer below.

• Optimisation of cardiopulmonary function
• Assistance in the weaning process utilising ventilatory support and oxygen therapy
• Instigation of an early rehabilitation/mobilisation program to assist in preventing the consequences of enforced immobility
• Advise on positioning to protect joints and to mini-mise potential muscle, soft tissue shortening and nerve damage
• Optimisation of body position to effect muscle tone in the brain-injured patient
• Optimisation of voluntary movement to promote functional independence and improve exercise tolerance
• Management of presenting musculoskeletal pathology
• Advise and education of family and carers
• Liaison with medical and nursing staff on the continuation and monitoring of ongoing physiotherapy-devised care plans.

A more structure list-like answer would resemble the following:

• Respiratory optimisation
  • manual hyperinflation, suction, inspiratory muscle training, positioning, percussion/vibration
• Musculoskeletal optimisation
  • Mobilisation, joint-protective positioning, tone-improving positioning
• Orthopedic
  • Management of immobilisation devices, application and removal of plaster casts, fitting of collars, braces and slings
• Rehabilitation
  • Exercise and education to improve function following a period of critical illness

At some point, the cynical candidate should use a key phrase such as "multidisciplinary team", "collaborative interdisciplinary care" or "shared therapeutic strategy". 

Potential risks of physiotherapy:

• Airway trauma from suctioning
• Deterioration in gas exchange
• Barotrauma
• Paradoxically, chest physiotherapy can actually increase the duration of ventilation (Maie et al, 2007)
• Haemodynamic instability
• Increased cardiac output requirements
• Rise in ICP
• Increased patient pain, stress and anxiety
• Risk of falls
• Pressure areas from splints
• Wound dehiscence (eg. of laparotomy wounds)

References

Oh's Manual (7th ed) Chapter 5 (pp.38)  Physiotherapy  in  intensive  care   by Fiona  H  Moffatt  and  Mandy  O  Jones

Stiller, Kathy. "Physiotherapy in intensive care: towards an evidence-based practice." CHEST Journal 118.6 (2000): 1801-1813.

College Answer

• Loss of comet tails and “marching ants” appearance
• Ribs and pleura move together
• “Lung point” – motionless horizontal lines are replaced by normal lung appearance moving from non-dependent to dependent region and also seen with inspiration and the probe held stationary.
• Loss of “waves on the beach” appearance in M-mode

Discussion

This is one of those things which is better explained with pictures.

In dry boring words, there is a list of features which one can easily memorise:

1. Absence of "Seashore sign" on M-mode
2. Absence of "B-lines" or "comet-tails" moving in synchrony with the pleura
3. Absence of sliding lung
4. Lung point sign - the point where the pneumothorax transitions into normal lung

References

Husain, Lubna F., et al. "Sonographic diagnosis of pneumothorax." Journal of Emergencies, Trauma & Shock 5.1 (2012).

College Answer

a)
Musculoskeletal
 Limited neck mobility
 Cervical spine instability
 Limited mouth opening (TMJ)
 Cricoarytenoid arthritis
 Chest/spinal deformity
Pulmonary
 Underlying lung disease – e.g. ILD – further reducing her respiratory reserve
Cardiac
 Underlying cardiac disease – cardiac failure, IHD, valvular disease.
 May influence choice of induction agent(s).
Metabolic
 Impaired renal, hepatic function – more likely from medications for RA.
 May influence choice of induction/paralysing agents.

b) 
Related to the RA itself 
 RA can be a multisystem disease. 
 Respiratory – pulmonary fibrosis, pleural effusion, reduced chest wall compliance. 
 Cardiac – increased risk of IHD, pericardial disease, valvular insufficiency, cardiac failure. 
 Renal – insufficiency directly related to the RA is rare, although does occur (GN, IN, amyloid). 
 Haematological – e.g. anaemia (chronic disease), thrombocytopenia (Felty’s). 
 Amyloidosis – cardiac, renal, hepatic. 
 Skin / pressure sores. 
 Difficult venous / arterial access – limb deformity. 
 Analgesia requirement. 
 Secondary amyloidosis affecting liver spleen and kidneys. 
 Decisions re-extubation if difficult intubation. 
 Post-extubation – difficulties with chest physiotherapy, mobilisation. 
 Psychosocial aspects of patient with chronic illness.

Related to the treatment for RA 
 Immunosuppression – infectious complications. 
 Other cytopaenias – anaemia, thrombocytopenia. 
 Need for adequate steroid replacement if long-term use. 
 Pulmonary – e.g. ILD from MTX, gold. 
 Renal – more likely related to medications that RA itself – e.g. NSAIDS, cyclosporine, penicillamine, gold. 
 Hepatic – e.g. MTX, Azathioprine. 
 Upper GI bleeding – NSAID, SSZ use. 
 Myopathy, skin breakdown, hyperglycaemia – steroids. 
 Drug interactions.

Examiners' comments: Candidates did not think broadly enough, e.g. in part (a) confined their answer to issues relating to C-spine disease.

Discussion

1. Difficult intubation, as caused by the belowmentioned issues:
   1. Poor neck extension due to C-spine arthritis
   2. Risk of spinal cord injury due to atltantoaxial subluxation
   3. Poor mouth opening due to TMJ arthritis
   4. Poor vocal cord opening due to laryngeal arthritis or crico-arytenitis
   5. Poor respiratory reserve due to pulmonary fibrosis
   6. Difficulty assessing all of these issues in the context of an ICU intubation - you are not seeing this person in the pre-admission clinic; likely they are trying to die in some sort of advanced life support scenario.
2. Difficult mechanical ventilation:
   1. Oxygenation pproblems:
      1. Pulmonary fibrosis, diffusion defect
      2. Pulmonary hypertension
   2. Ventilation problems
      1. Pleural effusions
      2. Restrictive lung disease with poor complicance
   3. Weaning problems:
      1. Poor muscle strength due to steroid myopathy
      2. Delayed extubation if the intubation was difficult
3. Cardiac and vascular problems:
   1. Propensity to arrhythmias
   2. Increased risk of ischaemic heart disease
   3. Diastolic failure due to restrictive cardiomyopathy and pericardial disease make fluid resuscitation challenging
   4. Cardiac weirdopathy (eg. failure due to amyloid deposition needs to be considered in the differential diagnosis of an otherwise unexplained heart failure when the patient also has RA)
   5. Difficult vascular access (limb deformities)
   6. Poor mobility and deformity promotes the development of pressure areas
4. Neuropsychiatric problems:
   1. Steroid-induced psychosis - extubation may be interesting
   2. Psychological problems of chronic disease
   3. Increased analgesic requirements (chronic opiate/NSAID use)
5. Electrolyte and endocrine abnormalities associated less with RA than with its treatment:
   1. Chronic steroid use may promote hypoadrenalism
   2. Electrolyte derangement due to chronic steroid use
6. Renal problems:
   1. RA-associated (eg. glomerulonephritis, amyloidosis)
   2. Treatment-associated (eg. NSAID-induced damage)
   3. Does one commit to long term dialysis in this setting?
7. Gastrointestinal and nutritional problems:
   1. "Rheumatoid cachexia" due to cytokine-driven hypermetabolism promotes the need for more protein and calories (Roubenoff et al, 1994) - but it is unclear whether they benefit from "overfeeding", as they tend to become cachexic in spite of a theoretically adequate dietary intake.
   2. Gastic erosion/ulceration due to chronic steroid and NSAID use suggests that this group should get PPIs routinely
8. Haematological disturbances
   1. Anaemia of chronic disease: will you transfuse them?
   2. Thrombocytopenia (Felty's) - increased risk from neuraxial procedures and vascular access
9. Immune and infectious issues
   1. Increased risk of infection
   2. Increased propensity to be often seen in hospitals tends to result in increased risk of MRO colonisation
   3. Weird antiRA drugs may interact with antibiotics

References

​Talley and O'Connor is a good source for the clinical features of RA.

Arnett, Frank C., et al. "The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis." Arthritis & Rheumatism31.3 (1988): 315-324.

Chanin, Katia, et al. "Pulmonary manifestations of rheumatoid arthritis." Hospital Physician 37.7 (2001): 2328.

Grassi, Walter, et al. "The clinical features of rheumatoid arthritis." European Journal of Radiology 27 (1998): S18-S24.

Krane, S. M., and L. S. Simon. "Rheumatoid arthritis: clinical features and pathogenetic mechanisms." The Medical clinics of North America 70.2 (1986): 263-284.

Canelli, Robert, John P. Weaver, and Elifce Cosar. "Anesthetic Considerations for Cervical Fusion Surgery in Advanced Rheumatoid Arthritis and Severe Pulmonary Hypertension." (2012).

Roubenoff, Ronenn, et al. "Rheumatoid cachexia: cytokine-driven hypermetabolism accompanying reduced body cell mass in chronic inflammation." Journal of Clinical Investigation 93.6 (1994): 2379.

McInnes, Iain B., and Georg Schett. "The pathogenesis of rheumatoid arthritis." New England Journal of Medicine 365.23 (2011): 2205-2219.

Samanta, R., K. Shoukrey, and R. Griffiths. "Rheumatoid arthritis and anaesthesia."Anaesthesia 66.12 (2011): 1146-1159.

College Answer

a)
Pressure area ulcer

b)
Duration of surgery
Faecal incontinence and/or diarrhoea
Low albumin concentrations
Disturbed sensory perception
Obesity
Moisture of the skin
Impaired circulation
Use of inotropic drugs
Diabetes mellitus
Too unstable to turn, or other reason for decreased mobility,
High APACHE II score. Waterlow’s score, Braden’s score or other valid scores

c)
Remove all pressure from area
Appropriate wound management
Plastic surgical review
Adequate nutrition
Wound nurse team.
Bowel management system.

d)
Maintaining clean and dry skin
Visualise skin integrity twice a day
Regular pressure relief and pressure relief mattresses

Discussion

Yep, that's a pressure area.

This question is essentially a repat of Question 29.2 from the first paper of 2009,  Question 7 from the first paper of 2007 and Question 2d  from the first paper of 2003.

Risk factors

Modifiable risk factors

• Prolonged immobility
• Use of neuromuscular junction blockers
• Use of steroids
• Hemodynamic instability preventing pressure area care
• Incontinence with soiling
• Low albumin
• Poor nutrition
• Oedema
• Hypotension

Non-modifiable risk factors and comorbidities

• Low BMI (no padding!)
• Altered mental state
• Peripheral vascular disease
• Diabetes
• Age over 60
• Severe illness (APACHE II score over 13)

Associated disease states:

• malignancy
• stroke
• pneumonia
• sepsis
• heart failure

Management

• Engagement of a multidisciplinary wound care team
• Debridement
• Antibacterial (silver sulfadiazine) dressings
• Frequent dressing changes
• Exudate-absorbing dressings
• Promote wound healing:
  • Adequate nutritional supplementation, particularly of protein (2g/kg/day)
  • Control of diabetes
  • Avoidance of corticosteroids
  • Optimisation of tissue perfusion
  • Avoidance of oedema

Prevention

• Use of a "skin integrity care bundle", for example the InSpPiRE protocol (Coyer et al, 2015)
• Risk assessment and monitoring
• Mobility
• Minimise sedation and restraints to allow for self-repositioning
• Management of incontinence (rectal pouches, IDC)
• 2 hourly repositioning
• Air mattress or specialised foam (evidence is not strong)
• Adequate skin care (clean and dry)
• Adequate nutrition
• Control of modifiable risk factors (eg. hypotension, oedema, low albumin, steroids)

References

Keller, Paul B., et al. "Pressure ulcers in intensive care patients: a review of risks and prevention." Intensive care medicine 28.10 (2002): 1379-1388.

Cullum, N., et al. "Beds, mattresses and cushions for pressure sore prevention and treatment." The Cochrane Library (2000).

REULER, JAMES B., and THOMAS G. COONEY. "The pressure sore: pathophysiology and principles of management." Annals of Internal Medicine94.5 (1981): 661-666.

Health Quality Ontario. "Pressure Ulcer Prevention: An Evidence-Based Analysis." Ontario health technology assessment series 9.2 (2009): 1.

Stratton, Rebecca J., et al. "Enteral nutritional support in prevention and treatment of pressure ulcers: a systematic review and meta-analysis." Ageing research reviews 4.3 (2005): 422-450.

Henzel, M. Kristi, et al. "Pressure ulcer management and research priorities for patients with spinal cord injury: consensus opinion from SCI QUERI Expert Panel on Pressure Ulcer Research Implementation." J Rehabil Res Dev 48.3 (2011): xi-xxxii.

Theaker, C., et al. "Risk factors for pressure sores in the critically ill."Anaesthesia 55.3 (2000): 221-224

Krupp, Anna E., and Jill Monfre. "Pressure Ulcers in the ICU Patient: an Update on Prevention and Treatment." Current infectious disease reports 17.3 (2015): 1-6.

Coyer, Fiona, et al. "Reducing Pressure Injuries in Critically Ill Patients by Using a Patient Skin Integrity Care Bundle (Inspire)." American Journal of Critical Care 24.3 (2015): 199-209.

College answer

a) Definition: 
The acute onset of a disturbance of consciousness with inattention, changes in cognition and/or perception, that fluctuates over time, occurs as a consequence of a general medical condition and is not better accounted for by a pre-existing, established or evolving dementia. 

b) Causes / Predisposing factors:

• Age >80
• Pre-existing cognitive impairment
• Severity of illness
• Visual impairment
• Dehydration
• Infection/Fever/Hypothermia
• Hypoxia
• Drugs/Polypharmacy o Esp Psychoactive drugs o Anticholinergics,  o Narcotics o Steroids
• Drug withdrawal  o Etoh, Benzos, SSRI
• Metabolic shifts- [Na], renal failure, BSL, Wernickes
• Cardiorespiratory disease
• Sensory deprivation, overstimulation
• Trauma/Post op o Esp – Cardiac sx, Cataract sx, Orthopedics and TURP   

 c) Assessment:

• DSM V
• CAM, CAM ICU
• Memorial delirium assessment scale

d) Treatment

• High-level supportive care 
• Sleep hygiene
• Hydration
• nutrition- thiamine
• Early mobilization
• Avoid physical restraints
• Visual and hearing aids
• Minimize staff changes and utilize family members
• Frequent reorientation
• Do not directly engage or oppose hallucinations/ paranoid behaviours
• Treat underlying cause and precipitant
• Treat psychotic phenomenology
• Haloperidol
•  Risperidone
• Olanzapine
• Dexmetomidine 

Additional Examiners Comments
In general, well answered.

Discussion

This question closely resembles Question 29 from the second paper of 2009. It also features a positive comment from the examiners, which is unprecedented.

a) Definition of delirium (the DSM V definition)

• Disturbance in attention (ie, reduced ability to direct, focus, sustain, and shift attention) and awareness.
• Change in cognition (eg, memory deficit, disorientation, language disturbance, perceptual disturbance) that is not better accounted for by a preexisting, established, or evolving dementia.
• The disturbance develops over a short period (usually hours to days) and tends to fluctuate during the course of the day.
• There is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by a direct physiologic consequence of a general medical condition, an intoxicating substance, medication use, or more than one cause.

b) Risk factors:

c) Management of delirium

Non-pharmacological:

• Good analgesia
• Clear and firm communication with the patient
• Frequent re-orientation
• Family presence
• Low-noise environment
• Restoration of hearing aids and spectacles
• Avoidance of sleep disturbance, promotion of normal sleep–wake cycle.
• Avoidance of physical restraints
• Early removal of IV lines and IDC
• Early mobilisation
• Adequate hydration
• Adequate (oral) nutrition
• Use of thiamine

Pharmacological:

• Dexmedetomidine
• Atypical antipsychotics
• Classical antipsychotics
• Benzodiazepines (if withdrawing from alcohol or benzodiazepines)

References

Oh's Intensive Care manual: Chapter 49   (pp. 549) Disorders  of  consciousness  by Balasubramanian  Venkatesh

Girard, Timothy D., Pratik P. Pandharipande, and E. Wesley Ely. "Delirium in the intensive care unit." Critical Care 12.Suppl 3 (2008): S3.

Barr, Juliana, et al. "Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit." Critical care medicine 41.1 (2013): 263-306.

Ouimet, Sébastien, et al. "Incidence, risk factors and consequences of ICU delirium." Intensive care medicine 33.1 (2007): 66-73.

Van Rompaey, Bart, et al. "Risk factors for intensive care delirium: a systematic review." Intensive and Critical Care Nursing 24.2 (2008): 98-107.

Schweickert, William D., et al. "Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomised controlled trial."Lancet (London, England) 373.9678 (2009): 1874-1882.

Inouye, Sharon K., et al. "A multicomponent intervention to prevent delirium in hospitalized older patients." New England journal of medicine 340.9 (1999): 669-676.

College answer

• Frontal baldness
• Myotonic facies
• Wasting of facial muscles, sternocleidomastoids, muscles of distal extremities
• Myotonic spasms (e.g. delay in opening fingers after making a fist)
• Percussion myotonia
• Cardiomyopathy
• Cataracts
• Testicular atrophy
• Slurred speech (pharyngeal myotonia)
• Intellectual impairment
• Absent reflexes

Discussion

What a weird thing to ask about. Myotonic dystrophy is a  congenital disorder which results in an abnormal skeletal muscle myosin kinase protein. The college answer lists 11 features, but in fact there may be many more. An excellent review by Turner et al (2010) adds a few extra features.  Remixed with the college answer, the full list looks like this:

References

College answer

a)

Acromegaly

b)

Hyperglycaemia (Diabetes mellitus)
Hypercalcaemia
Hypercalciuria
Low cortisol
Hypernatraemia (diabetes insipidus)

Discussion

Now, I don't want to get into any sort of legal trouble by reproducing the images which the college decided to withhold as a part of their "official" papers, but reliable sources report that the images used in this question were ripped straight from Wikipedia. Instead of re-using these images (which would arguably be completely legitimate, as they are covered by essentially the same Creative Commons license as the rest of this site) I have sourced others. In case one requires the college originals, they can be viewed in Chanson et al (2008). 

The images I have used came from this weird alterna-health website where annoying popups tried to warn me about "Never Eat These Three Fatigue-Causing Foods" etc. Clearly these authors are not the original source of the photographic progression of male faces, which demonstrate the gradual changes associated with acromegaly. The hand pictures came from another severely ad-polluted site (Medindia.com). I hope these are unequivocal. No other answer should be possible for a).

b) affords more variation. Acromegaly is associated with a whole host of clinical features, of which biochemical abnormalities are only one part. Molitch (1992) lists a whole lot of these, but the article is paywalled. Instead one can get Melmed Shlomo's 2006 NEJM piece from tripod.com. It's just as good. In fact there is a table (Table 1, Clinical Features orf Acromegaly) which lists everything you could ever think of which might be associated witht his disease, from the local effects of pituitary adenoma to things like narcolepsy and galactorrhoea. The whole table is reproduced here.

References

College answer

Call for help: Hospital emergency response (Code Black or equivalent)

 May be a medical illness (hypoxia, hypoglycaemia, metabolic disturbance), psychiatric disorder (acute psychosis, drug-induced psychosis, delusional state, mania or personality disorder) or drug intoxication or withdrawal causing the aggressive violence.

 Sedation to gain control of the situation may be required to allow such an assessment.

Acute Management

 De-escalation, containment and negotiation techniques if appropriate and most likely to work in a situation of low level threat (unlike this one).

Physical restraint – to allow delivery of drug therapy, need help / security team / police etc.

Chemical restraint:

i. Options:

1. Benzodiazepines:
   1. Diazepam / Midazolam / Lorazepam
   2. Advantages of rapid action, good safety profile
   3. Concern: Sedation / Drowsiness / Respiratory depression / hypotension/short acting
2. Anti-psychotics:
   1. Typical
      1. Haloperidol
      2. Droperidol (increasing profile for relatively safe emergency sedation)
   2. Atypical
      1. Olanzepine ii. Risperidone

1. 3. Advantages – less respiratory depression, can be given im.
   4. Concerns: Extra-pyramidal side effects / QT prolongation / hypotension /slow onset, may require repeated administration

3. NMDA-antagonist (Ketamine):
   1. Advantage: Can be given im, much less respiratory depression or hypotension, rapid onset
   2. Concern: Hallucinations / Hypertension, tachycardia / 

4. Intravenous anaesthetic agents (propofol, thiopentone)
   1. Advantage – very rapid action with guaranteed effect
   2. Concerns – apnoea, hypotension. May require intubation.

(B) Post-intervention considerations.

1. Assessment and investigation for medical / psychiatric cause of severe agitation
2. Adequate monitoring and support of vital signs
3. Monitoring for adverse effects of medications used to control the individual
4. Examination for injuries to the perpetrator
5. Documentation
6. Debrief – staff involved / perpetrator, when calm and rational other patients, perpetrator’s family
7. Disposition – monitored environment

Examiner Comments:

Most candidates omitted thinking about or looking for causes of aggression (e.g. hypoxia) and did not mention any post-intervention considerations.

Discussion

This is far from uncommon, and the level of detail invested into the scenario suggests that some lightly bruised veteran of the ICU wrote the question in memory of a particularly extreme confrontation. Fortunately, there is a NSW Health directive to guide this area of practice.

Ensuring safety of the patient and staff 

• Retreat to a safe place; remove staff to a safe area or to a safe distance, as much as possible
• Activate duress alarm
• Activate local emergency response (usually designated Code Black)

De-escalation technique

• An attempt to de-escalate the situation by engaging with the aggressive patient is one option, Some techniques have been suggested:
  • Respecting personal space
  • Appropriate body language using a non-confronting manner
  • Establishing appropriate verbal contact to engage with the person
  • Communicating in a clear and concise manner, avoiding repetition
  • Listening and acknowledging the person’s concerns
  • Identifying the person’s needs and feelings 
  • Setting clear limits and boundaries
  • Being respectful
  • etc etc
• Defusing the situation through conversation seems like an appropriate place to start. 
• However this would probably not be a reasonable thing to include in the answer to Question 27. Specific offensive behaviours were quoted by the college, likely as a means of communicating to the trainees that they were not dealing with a reasonable person. If the patient is headbutting the staff, we are probably no longer in conversation territory. 

Physical behavioural control measures

• The security team needs to nominate the team leader
• The team leader should assigns roles for each staff member
• One staff member should support or hold each limb
• One staff member should support or hold the head and continue to engage with the patient to "reassure and calm" them while they bite and spit.
  With the patient physically restrained, it may now be possible to administer chemical restraints.

Chemical behavioural control measures

• In Question 27 from the first paper of 2018, the college wanted a list of drugs and their advantages/disadvantages. To quote several classes and to write "sedation/drowsiness/respiratory depression" as the disadvantage for all of them would probably win few marks. All these drugs have "rapid onset|" as an advantage and "sedation/drowsiness" as a disadvantage because you are using them to rapidly sedate somebody. Thus, the following list is offered with the intention of making these drug classes look so sufficiently different that the choice of which drug to give is not rendered meaningless.
  • Benzodiazepines: Midazolam, diazepam, lorazepam, clonazepam
    • Advantages:
      • Rapid onset of effect
      • Safe to give IM
    • Disadvantages
      • When given IM, unpredictable pharmacokinetics
      • Prolonged duration of action and delayed peak effect may give rise to an inadvertent overdose ("he just won't stay down, give him more!")
      • Some of these patients may be multi-drug resistant organisms and may  be recreationally taking substantially more benzodiazepines than you would ever be willing to inject into them for behaviour control.
  • Classical antipsychotics: haloperidol, droperidol
    • Advantages:
      • Relatively short duration of action
      • Significant experience with their use
      • System-level support is strong- eg. many Australian health services have adopted droperidol as their drug of choice following the hilariously titled DORM trial (Isbister et al, 2010)
    • Disadvantages:
      • QT intervals will become prolonged with excess use
      • Extrapyramidal side effects may produce motor problems which may extend to such unpleasantness as respiratory arrest due to muscle rigidity
      • Most of these drugs are alpha-1 antagonists, which will cause hypotension
      • Anticholinergic side efects cause urinary retention and may exacerbate delirium
  • Atypical antipsychotics
    • Advantages:
      • Generally viewed as safer than the classical agents
      • Less anticholinergic and other side effects
      • Longer duration of action for sustained effect
    • Disadvantages:
      • Many agents are not available in IV/IM formulations, which means you will be relying on some degree of cooperation, to swallow the tablet.
      • Slow onset of antipsychotic effect; immediately useful effect is actually an antihistamine-like sedation which is probably no different to the classical agents in mechanism, except slower. 
  • Dissociative anaesthetics
    • Ketamine has been suggested as an agent for the "difficult to control" aggressive patients who have already had dangerous doses of other drugs. Data on this were publsihed by Isbister et al (2016), who gave their patients  a median dose of 300mg (!) of ketamine to chase the 25mg of droperidol which they have already had.
    • Advantages:
      • Airway reflexes are preserved
      • it is another class to use in a multimodal approach to behaviour control
    • Disadvantages:
      • Psychosis may get worse
      • The patient may hallucinate
      • Analgesic effect renders the patient immune to pain, which may result in self-harm
      • Agitation associated with ketamine may be difficult to distinguish from the pre-existing agitation 
  • General anaesthetics
    • The college answer to Question 27 recommends barbiturates or propofol, quoting rapid action and a "guaranteed" effect. One might also make the argument that 500mg of intramuscular suxamethonium might be similarly rapid in onset, and offer a similar certainty of behaviour control. 
    • Propofol has been used as an infusion in these cases (Chalwin et al, 2012)- apparently only 30-50mg/hr was required to sustain "conscious sedation, leading to satisfactory patient compliance with healthcare interventions".
    • The natural tendency of these situations to lead to intubation needs to be mentioned.

Investigations and post-sedation care

• Determine need for ongoing physical restraints
• Monitor vital signs
• Examine the patient for injuries
• Explore organic differentials (eg. meningitis, encephalitis, head trauma, hypoxia, pain, background of developmental delay, metabolic encephalopathy)

Post-event care of staff and family

• Debrief with staff
• Discussion with patient's family
• Escalation of incident to incident monitoring committee
• Institution-level interventions (eg. aggression management workshops and training in safe "take-down" techniques of physical restraint)

References

College answer

a)    Infections:  
Viral e.g. Influenza, Coxsackie, Mumps 
Bacterial e.g. GAS, Diphtheria, Mycoplasma 
 
Drugs: 
Sulfonamides 
Beta-lactams 
Anti-convulsants 
NSAIDs 
Allopurinol 
Paracetamol 
 
Malignancy 
 
b)    General: 
Multi-disciplinary approach with dermatology, plastics, ophthalmology. Best managed in specialised burns unit 
Stop precipitating agents e.g. NSAID / allopurinol General Haemodynamic and respiratory support. 
Reverse-Isolation in single room with room temperature increased to 30-320C. 
Awareness of potentially high fluid loss: may require aggressive replacement 
Wound care: Cover the denuded skin with anti-septic soaked dressings, vigilance for secondary skin infections. No role for prophylactic antibiotics. 
Analgesia for painful skin lesions and for dressing change. 
Eye care: look for conjunctival hyperemia, epithelial defect & pseudomembrane formation. Treat with topical lubricants, topical steroids and topical antibiotic, as guided by ophthalmology. Attempt to place lines through normal skin if possible 
 
Specific: 
Cyclosporin: Early administration at the dose of 3-5mg/kg is beneficial and is recommended.
Steroids: The use of systemic corticosteroids has not been evaluated in clinical trials & remains controversial. Early observational studies indicated higher frequency of complications & death; but recent meta-analysis found that steroid treatment was associated with reduced risk of death. The dose, route, duration & timing of steroids remain uncertain.  
Plasmapheresis: Reported to be beneficial in small series and case reports, but role still not well defined. 
Anti-TNFα monoclonal antibodies e.g. infliximab has been used successfully in small series of patients, but not recommended. 
 

Discussion

It is remarkable that this SAQ on a relatively rare condition had a 58% pass rate. The last time toxic epidermal necrolysis came up (in Question 10 from the first paper of 2005), only 13% of the candidates passed. Presumably, of that 34-candidate cohort from 2005 (of whom 19 were successful), thirteen years later some proportion were senior college fellows and Part II examiners, and now they think this question is a really good idea from an assessment value standpoint.

The best literature for the management of TEN is unfortunately paywalled (Fromowitz et al, 2007). That particular article shines brightest because they incorporate a long (28-point) list of management recommendations from the University of Florida protocol. Fortunately, Schneider & Cohen have an even better article, which is more recent (2017). Additionally, the 2016 UK guidelines are available as a free PDF (Creamer et al, 2016).  These and other resources have been remixed and recut into the summary below.

• Supportive management:
  • A- Intubation is almost inevitable because of the sedation and analgesic requirements
  • B- Wherever mechanical ventilation can be avoided, humidified oxygen is preferred to regular wall oxygen because of the mucosal injuries
  • C- Expect a hyperdynamic vasodilated circulation with hypovolemia:
    • Replace lost fluid (see F below)
    • Vasopressors to maintain MAP targets
    • Use PICC access (anticipating long term IV access requirements with few normal patches of skin available for PIVCs and CVCs)
    • Beware of line dressings. Where possible, avoid adhesive dressings.
  • D - Expect complex pain needs:
    • The patient will likely require a multimodal approach to analgesia with some combination of IV opiate and opiate-sparing agents like ketamine. For dressing changes, expect to need either general anaesthetic, ketamine sedation or methoxyflurane.
    • Psychological support will be required to the patient and family (disfiguring illness, prolonged ICU stay, extreme pain - all the recipes for PTSD and depression)
  • E - Expect electrolytes to be deranged:
    • Hypernatremia due to water loss
    • Hypophosphataemia due to large-scale tissue regrowth
  • F - Not quite a burns-like fluid management strategy: fluid requirements are usually about 30% lower than for burns of a similar extent (Schenider & Cohen, 2017)
    • Replace large volumes of crystalloid, using a balanced crystalloid
    • Haemoconcentration is a guide to replacement adequacy
    • Albumin replacement will be required due to ongoing protein loss through wounds
  • G - Nutrition needs will be complex:
    • High caloric requirements, like sepsis (probably 125% of predicted) but lower than burns of a similar extent
    • High protein requirements (2.0-2.5g/kg/day) to account for losses and hypercatabolic state
    • Expect oral diet to be impossible owing to mucosal injuries; expect these injuries to frustrate NG placement. Early placement of a feeding NG tube is vitally important.
    • Anticipate constipation due to high dose opiates
    • Ensure vigorous ulcer prophylaxis (high dose steroids will be used)
    • High risk for C.difficile infection (likely, broad spectrum antibiotics will be used)
  • H - Expect the patient to be at high risk of VTE:
    • Chemical thromboprophylaxis needs to be fastidious, as there is usually nowhere to place TEDs and calf compressors
  • I - Infectious diseases specialists need to be included in decisionmaking. Broadly:
    • Antibiotics are not indicated unless there is a clinically evident infection
    • Topical antibiotics for conjunctiva are indicated (chloramphenicol)
    • Antibiotic-coated lines are indicated (especially if placed through affected skin)
    • If somebody started steroids, stop them.
• Specific management:
  • The following therapies are all largely based on case series or expert opinion. Representative articles are included for reference.
    • Cyclosporin (Arevalo et al, 2000)
    • Corticosteroids (thought to be useless - Schneck et al, 2008)
    • IV immunoglobulin decreases mortality (Barron et al, 2015)
    • Plasmapheresis (some positive results from Han et al, 2017)
    • Anti-TNFα monoclonal antibodies (case reports, eg. Hunger et al, 2005)
    • Thalidomide (potentially detrimental - Wolkenstein et al, 1998)

References

College answer

Discussion

Though some might say that a test of analytic capabilities is more important, it is clearly still relevant for the college to make sure their trainees have strong semantic memory, even though more recently data storage has been extensively outsourced to external structures such as the Internet. One may still argue that the 31.8% of trainees who were able to effortlessly recall these details would make slightly sharper intensivists. 

The nerve conduction findings in Guillain-Barre syndrome

Some very old diagnostic guidelines from 1990 (Asbury & Cornblath)

• Nerve conduction slowing in 80% of cases at some point during the illness (velocity is usually less than 60% of normal), which is consistent with demyelination
• Specific characteristic findings:
  • Partial conduction block
  • Decreased M-responses
  • Temporal dispersion
  • Prolonged distal latencies
  • Prolonged or absent F waves and H-reflexes
• 20% of cases have normal conduction studies
• Sensory conduction studies are occasionally abnormal (reduction in evoked amplitude)
• Axonal disease features absent or severely reduced compound muscle action potential amplitudes, with preserved conduction velocities

The cerebral spinal fluid findings in Listeria meningitis

The lymphocyte-rich CSF in Listeria meningitis can occasionally confuse a young player, where "the unwary may dismiss lymphocytic meningitis as being of 'viral' origin", according to an old paper by Hearmon & Ghosh (1989). It is otherwise classical bacterial meningitis (low glucose, high CSF protein, and of course characteristic Gram-postive rods of which there are not many). 

MRI features in posterior reversible encephalopathy syndrome (PRES)

As listed by Bartynski (2008):

• T1: hypointense in affected regions
• T1 C+ (Gd): patchy variable enhancement. It can be seen in ~35% of patients, whether leptomeningeal or cortical pattern.
• T2:  hyperintense in affected regions
• DWI: usually normal
• ADC: signal increased in affected regions due to increased diffusion
• GRE: may show hypointense signal in cases of haemorrhage
• SWI: may show microhemorrhages 

Full blood count and blood film in Vitamin B12 deficiency

This is from Snow (1999) and UpToDate:

• Macrocytosis - the MCV tends to increase before anaemia develops. Only a truly massive MCV is sensitive for B12 deficiency (over 130 fL).
• Hypersegmented neutrophils also precede anaemia - this is the presence of at least one neutrophil with at least 6 lobes or more
• Anaemia is usually hypochromic and macrocytic
• Leucopenia/thrombocytopenia and low reticulocyte count reflect poor haematopoiesis
• Evidence of haemolysis may be present (eg. RBC fragments)

Plain cervical spine x-ray in ankylosing spondylitis 

As the practice of ordering plain C-spine radiographs has largely died out over 10 years ago, it is strange to find it in the 2019 paper, but here we are. From Radiopedia and Østergaard (2012):

• Romanus lesions of the spine (shiny corner sign): small erosions at the corners of vertebral bodies with reactive sclerosis
• vertebral body squaring
• Andersson lesion: noninfectious spondylodiscitis:
• Bamboo spine: diffuse syndesmophytic ankylosis 
• Dagger spine: interspinous ligament ossification
• enthesophyte formation from enthesopathy
• dural ectasia

References

College answer

References

Chanin, Katia, et al. "Pulmonary manifestations of rheumatoid arthritis." Hospital Physician 37.7 (2001): 2328.

Grassi, Walter, et al. "The clinical features of rheumatoid arthritis." European Journal of Radiology 27 (1998): S18-S24.

Krane, S. M., and L. S. Simon. "Rheumatoid arthritis: clinical features and pathogenetic mechanisms." The Medical clinics of North America 70.2 (1986): 263-284.

Canelli, Robert, John P. Weaver, and Elifce Cosar. "Anesthetic Considerations for Cervical Fusion Surgery in Advanced Rheumatoid Arthritis and Severe Pulmonary Hypertension." (2012).

Roubenoff, Ronenn, et al. "Rheumatoid cachexia: cytokine-driven hypermetabolism accompanying reduced body cell mass in chronic inflammation." Journal of Clinical Investigation 93.6 (1994): 2379.

McInnes, Iain B., and Georg Schett. "The pathogenesis of rheumatoid arthritis." New England Journal of Medicine 365.23 (2011): 2205-2219.

Samanta, R., K. Shoukrey, and R. Griffiths. "Rheumatoid arthritis and anaesthesia."Anaesthesia 66.12 (2011): 1146-1159.

College answer

References

Freeman, William D., et al. "ICU management of patients with Parkinson's disease or Parkinsonism." Current Anaesthesia & Critical Care 18.5-6 (2007): 227-236.

Vincken, Walter G., et al. "Involvement of upper-airway muscles in extrapyramidal disorders: a cause of airflow limitation." New England Journal of Medicine 311.7 (1984): 438-442.

Katus, Linn, and Alexander Shtilbans. "Perioperative management of patients with Parkinson's disease." The American journal of medicine 127.4 (2014): 275-280.

College answer

1. Interpret the blood gas. (2 marks)
   • High anion gap metabolic acidosis with respiratory compensation
   • Elevated Aa gradient 40mmHg (5.3kPa)
2. What is the most likely diagnosis? (2 marks)

• • HAPE = High altitude pulmonary oedema
  • HACE = High altitude cerebral oedema

3. What is the treatment would you institute in this patient? (6 marks)

General (2)

• • Supplemental oxygen
  • Descend to lower altitude

High altitude pulmonary oedema (2)

• • Prompt reduction of pulmonary artery (PA) pressure :
    • Limit physical exertion and cold exposure,
    • Non-invasive ventilation (CPAP)
    • Pharmacological therapies to decrease pulmonary artery pressures: Nifedipine, Sildenafil/Tadalafil (Phosphodiesterase inhibitors)
  • Diuretic therapy, nitrates, and morphine are no longer recommended and could be harmful

High altitude cerebral oedema (2)

• • Dexamethasone
  • Consider hyperbaric therapy
  • ICP management – MAP maintained, minimise venous hypertension, adequate sedation and osmotic therapy

References

Mehta, S. R., A. Chawla, and A. S. Kashyap. "Acute mountain sickness, high altitude cerebral oedema, high altitude pulmonary oedema: The current concepts." Medical journal, Armed Forces India 64.2 (2008): 149.

Basnyat, Buddha, and David R. Murdoch. "High-altitude illness." The Lancet 361.9373 (2003): 1967-1974.

Hackett, Peter H., and Robert C. Roach. "High-altitude illness." New England journal of medicine 345.2 (2001): 107-114.

Bhagi, Shuchi, Swati Srivastava, and Shashi Bala Singh. "High-altitude pulmonary edema." Journal of occupational health (2014): 13-0256.

Basnyat, Buddha. "High altitude cerebral and pulmonary edema." Travel medicine and infectious disease 3.4 (2005): 199-211.

Stuber, Thomas, and Yves Allemann. "High altitude illness-pathogenesis and treatment." SCHWEIZERISCHE ZEITSCHRIFT FUR SPORTMEDIZIN UND SPORTTRAUMATOLOGIE 53.2 (2005): 88.

College answer

Not available.

Discussion

a) Question 30.1 from the first paper of 2017 also asked for six clinical features of myotonic dystrophy. Fourtunately, there's plenty to choose from:

b)

One might expect that features suggestive of severity in chronic AR would be mainly features related to the effect of AR on cardiac function, not just generic features of AR

• LV dilatation (displaced apex, diffuse hyperdynamic impulse)
• Congestive cardiac failure (low blood pressure, peripheral oedema)
• Poor exercise tolerance
• Signs of widened pulse pressure (see below)
• An S3, suggestive of poor LV function

Generic features of AR are as follows:

• Chacteristic auscultatory findings:
  • Soft S1
  • Soft A2
  • An S3 if LV function is severely depressed
  • A systolic ejection sound due to abrupt aortic distension
• Signs of widened pulse pressure:
  • Corrigans sign
  • de Musset's sign 
  • Quincke's sign
  • Duroziez's sign 
  • Traube's sign
  • Mueller's sign
  • Becker's sign 
  • Hill's sign
  • Mayne's sign
  • Rosenbach's sign
  • Gerhard's sign

From the wording of the question, it is not clear that the trainees were expected to know what these signs were; i.e. to list the eponyms would have been enough to pass. Their meaning is discussed elsewhere, in case anybody is interested

c) Bilateral miosis with coma:

• Bilateral pontine lesions
• Bilateral thalamic lesions
• Metabolic encephalopathy
• Cholinergic drugs
  • Organophosphates
  • Myasthenia gravis drugs (the 'stigmines, eg. pyridostigmine)
  • Alzheimers nootropics (the 'pezils, eg. donepezil)
  • Sarin gas
• Non-cholinergic drugs:
  • Opiates
  • Barbiturates
  • GHB
  • Clonidine
  • GHB
  • Chloral hydrate
  • Valproate
  • Atypical antipsychotics
  • Phenothiazines

d) The latery medullural syndrome (Wallenberg syndrome) consists of the following classical findings:

• On the side of the lesion:
  • Facial sensory loss
  • Nystagmus
  • Horner's syndrome
  • Loss of gag reflex
  • Ipsilateral ataxia with a tendency to fall to the ipsilateral side
• On the contralateral side:
  • Pain and temperature sensory loss in the extremities
• Generally:
  • Vertigo
  • Nausea
  • Dysphagia

References

College answer

Not available.

Discussion

To scale new heights of grammar pedantry, the author could breed division by pointing out that it's Down syndrome, not Down's syndrome, but even professional and charity organisations seem to do this apostrophe thing, and so anyway: 

Airway features: 

• Increased risk from sedation due to a labile upper airway with weaker muscle tone and frequent laryngomalacia.
• A greater risk of aspiration, owing to muscular hypotonia
• Small mouth, large tongue - likely, intubation will be more difficult
• Atlantoaxial instability is reportedly very common, 15-30% of patients

Respiratory function:

• Morbidity and mortality from respiratory disease(eg. ARDS) is greater in the Down syndrome population. Increased susceptibility to oxidative stress is blamed. 
• Often, they have subpleural cysts, which can predispose them to pneumothoraces with high pressure ventilation
• Often there may be pulmonary hypertension; of particular interest is pulmonary vein stenosis, which is rare but hideous and with a very high early childhood mortality

Cardiovascular features:

• About 40-50% of these children have congenital cardiac abnormalities, and there's a fair spectrum of them, but the most common are ASDs and VSDs which can become cyanotic when pulmonary pressure increases (eg. in pneumonia)

Neurological features:

• Hypotonia, i.e. poor muscle tone, may become an issue with ventilator weaning
• Cognitive developmental delay may change the way you need to assess their neurology for extubation assessment

Endocrine associations

• Hypothyroidism is common among Down syndrome patients

Nutritional issues 

• Celiac disease is common; gluten-free NG feeds and oral diet may be necessary

Immune features

• For unclear reasons, these children have worse outcomes from sepsis and respiratory infections than the general population.

References

College answer

Not available.

Discussion

This question is the repeat of a repeat of a repeat, and is an absolute gift. The weary exam candidate should be able to relax, letting their pen produce a muscle-memory automatic answer while their mind wanders away to a less depressing place.

a) Definition of delirium (the DSM V definition)

• Disturbance in attention (ie, reduced ability to direct, focus, sustain, and shift attention) and awareness.
• Change in cognition (eg, memory deficit, disorientation, language disturbance, perceptual disturbance) that is not better accounted for by a preexisting, established, or evolving dementia.
• The disturbance develops over a short period (usually hours to days) and tends to fluctuate during the course of the day.
• There is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by a direct physiologic consequence of a general medical condition, an intoxicating substance, medication use, or more than one cause.

b) Prevention of delirium:

• Identification of at-risk patients
  • Pre-existing dementia
  • Hypertension
  • Alcoholism
  • High severity of illness at admission
• Control preventable risk factors:
  • Minimise the use/duration of urinary catheters
  • Minimise the use of restraints
  • Decrease the use of opiates (especially morphine)
  • Minimise the use of benzodiazepines (restrict to those who are withdrawing from drugs/alcohol)
  • Rationalise polypharmacy
  • Where possible, cease or reduce the dose of anticholinergic drugs
• Decrease deliriogenic stimuli of critical care environment:​​​​​​​
  • Is deliriogenic even a word?
  • Encourage mobility: early mobilisation is the most evidence-supported intervention to prevent delirium (
  • Minimise intrusive care during sleep, reducing sleep deprivation
  • Encourage normal sleep-wake diurnal cycle, sun exposure, make use of rooms with outward-facing windows for delirium-prone patients
  • Involve the relatives to calm the patient
  • Keep noise to a minimum (eg. silence internal room alarms, turn off loud devices such as the suction catheter)
  • Manage pain aggressively
  • Prevent constipation proactively
  • Watch electrolytes carefully (hypo/hypernatremia, hypo/hypercalcemia, uraemia, etc)
  • Give them back their hearing aids and spectacles as soon as practical
  • I they are intubated, minimise their sedation doses
• Treat underlying condition:
  • ​​​​​​​Hypoxia, hypercapnia, hypotension - obviously the reason for the ICU admission

References

College answer

Not available.

Discussion

a) Assessment of frailty:

• Multidimensional assessment, consisting of:
  • History, eg. self-reported exhaustion, fatigue, mood, social participation
  • Proxy functional assessment, eg. use of mobility equipment, reliance on services, hospital admissions, frequency of falls
  • Functional disability assessment, eg. hand grip, gait, balance, cognitive assessment
  • Biometric data, eg. weight loss, muscle mass
  • Physical examination findings, for example:
    • Sarcopenia
    • Clinical features of malnutrition
    • Evidence of decreased energy expenditure
    • Features of multiple health deficits or comorbidities
  • Objective biological findings eg. echo findings, chronic organ system dysfunction, low serum prealbumin, etc.
• Use of a validated frailty scoring scale is recommended:
  • Numerous scales are available (see De Vries et al, 2011)
  • The CFS (Clinical Frailty Scale) is the one most commonly used in critically ill patients (Falvey & Ferrante, 2019)

b) Limitations of this assessment at the time of ICU admission:

• Assessment of frailty in general:
  • There may only be limited information regarding baseline function
  • Clinical features of frailty may be exaggerated by critical illness
  • Frailty may be absent on admission, but can then develop during the ICU stay
• Assessment using a fraily scoring scale:
  • There may be no time to use a comprehensive scoring scale
  • The use of such scales requires training
  • They are validated only among stable community outpatients
  • Their reliability is poorly studied (De Vries et al, 2011)

c) Utility of a frailty score in the management of critically ill patients:

• Prevention of non-beneficial therapies:
  • Frail patients have poorer ICU outcomes. 
  • High frailty scores are associated with discharge into residential care facilities,  medium to long term disability, and poor quality of life
  • Screening for frailty can be used as a prognostic indicator to inform decisionmaking around the goals of care and limitations of therapy
• Triage of critical care services
  • Under scenarios of system stress (eg. a pandemic response), frailty scoring may be a valid mechanism of allocating access to scarce critical care resources
• Redirection of clinical priorities: increased clinician attention to management strategies designed to maximise the preservation of function and the prevention of further enfeeblement, such as:
  • Nutrition (high caloric and high protein supplementation)
  • Micronutrient and vitamin replacement
  • Early extubation
  • Early mobility and physiotherapy
  • Delirium screening
  • Referral to services such as social work, psychology, occupational therapy and specialist geriatrician services

References