A 21-year-old with gunshot injuries to his head and abdomen has been in your ICU for three weeks. He has a GCS of 10 with a tracheostomy and is being weaned off mechanical ventilation. He develops a new onset fever of 39.0oC on day 22 in ICU. He has a sinus tachycardia at 120/min and has a BP of 100/70. A CT abdomen was performed and a representative cut of it is as seen.
Please describe the prominent findings on the CT image
The CT showed a pancreatitis with a possible abscess. The viva was a discussion on the management of a patient with acute pancreatitis.
Image attribution: Case courtesy of Dr Saeed Soltany Hosn, Radiopaedia.org. From the case rID: 20595
- non-enhancing low attenuating regions within the pancreas
- Suggestive of necrosis affecting the pancreatic head
What could be the cause of this?
There looks to be a small gallstone on that CT. However, it is not in the CBD. Other causes include:
- Alcohol (36%)
- Scorpion venom
- Gall stones (38%)
- Biliary tract disease
- Penetrating duodenal ulcer
- Atheroma (eg. post IABP insertion)
- Shock states
- End-stage renal failure
- Vasculitis (eg. SLE)
LITFL offers a nice mnemonic for these aetiologies: I GET SMASHED
- Gall stones
- Mumps and other viruses (EBV, CMV, HIV)
- Autoimmune diseases (SLE, polyarteritis nodosa, pregnancy)
- Scorpion stings
- Hypercalcaemia, hyperlipidaemia, hypothermia, hypotension (ischemia)
- ERCP, emboli
The patient becomes more tachycardic, and the blood pressure drops to 90/50. What is the underlying pathophysiology leading to these changes?
Causes of hypotension in pancreatitis:
- "Third space losses" due to capillary leak, particularly sequestration in the abdomen
- Systemic inflammatory response due to cytokine release
- Gastrointestinal losses due to vomiting, diarrhoea, decreased oral intake, and gastric bleeding
- Retroperitoeal haematoma (maybe from a ruptured splenic artery aneurysm)
- Decreased preload due to abdominal compartment syndrome
- Cardiac output decrease due to acidosis and SIRS-associated cardiomyopathy
How will you assess the patient?
- Clinically: examination of the chest, auscultation/percussion
- Examination of the ventilator waveforms
- Examination of the abdomen for distension
- EUC/CMP: low total calcium, renal failure,
- Arterial blood gas: ionised calcium, metabolic acidosis
- Amylase and lipase
- LFTs in the event the common bile duct is obstructed, and to screen for complications of alcoholism.
- Triglycerides to exclude that cause of pancreatitis
The abdomen is distended and tense to palpation. The air entry is significantly reduced in both lung bases. The urine output is 10ml/hr in the last 6 hours.
What complications do you think are taking place?
How would you confirm your diagnosis?
- Abdominal compartment syndrome
- Sepsis due to pancreatic abscess
- Mesenteric ischaemia
- Ascites due to portal vein thormbosis
- Abdominal compartment pressure
- Ultrasound of the portal circulation
- ABGs for lactate
- Surgical review
The nurse asks you to review the patient's ABG.
Please interpret these results, and give an explanation for the abnormal findings.
The ABG show:
- Hypoxia: A-a gradient 398 mmHg, PF ratio 77
This patient is hypoventilating because of increased intra-abdominal pressure and atelectasis.
The surgical team have suggested that there might be abdominal compartment syndrome.
What is the definition of this syndrome?
- Raised intra-abdominal pressure is a sustained or repeated pathological elevation in IAP≥12 mmHg.
- Abdominal Compartment Syndrome is deﬁned as a sustained IAP>20 mmHg that is associated with new organ dysfunction
What are the consequences of abdominal compartment syndrome?
- Decreased respiratory compliance, increased peak airway pressures
- Risk of pneumonia
- Decreased preload, thus hypotension
- Increased intracranial pressure
- Renal failure
- Mesenteric ischaemia, decreased intestinal mucosal perfusion
- Portal vein thrombosis
- Decreased gastric emptying, feed intolerance
- Lower limb venous thrombosis
How is abdominal compartment pressure measured?
- Empty the bladder
- Clamp IDC
- Attach noncompressible tubing and transducer
- Inject 20ml of fluid into the bladder
- Wait for the detrusor to relax (60 seconds)
- Zero the transducer to atmosphere, at mid-axillary line and at the level of the iliac crest
- Measure the pressure at end-expiration
- The measurement is valid under the following conditions:
- Patient is supine
- Muscle contraction is eliminated (eg. NMJ blockers)
What are the limitations of this method?
This resembles Question 10 from the second paper of 2001. Briefly, the following are reasons as to why one's intra-abdominal measurements may be wrong:
- Failure of technique
- Improper setup of the measuring set
- Improperly calibrated transducer
- Inappropriate zero point
- Leaking transducer system
- Confounding factors
- Increased pelvic pressure
- High detrusor tone
- Detrusor fibrosis
- Incompletely paralysed patient
What are the available management options?
- Avoid overvigorous fluid resusictation
- Vasopressors to maintain MAP within a certain range (some aim for an abdominal perfsion pressure of >60mmHg)
- Titrate PEEP to optimise V-Q matching, to maintain normoxia and normocapnea
- If compartment pressure remains elevated, neuromuscular blockade can be considered
- If pressure remains high in spire of NMJ blockade, may consider opening the abdomen (if it is closed)
The patient remains febrile (temp = 39.1° C). The surgical team have suggested that you start some broad spectrum antibiotics. What is your opinion of this?
- The answer should be "not for pancreatitis".
- Antibiotics should not be routinely given to patients with severe acute pancreatitis
- Clinical evidence of sepsis (including sepsis of other origin, eg. urinary or pulmonary) should be promptly treated with appropriate antibiotics (not pancreas-specific antibiotics)
- It may be possible to sample the collection by CT-guided aspiration; if the Gram-stain is positive this will be the deciding factor
What are the possible uses of antibiotics in severe acute pancreatitis?
- Prophylaxis to prevent infection of the necrotic pancreas
- Prophylaxis to prevent infection of the pancreatic pseudocyst
- Treatment of infected pancreatic necrosis
- Coincidental use of these antibiotics to treat an unrelated extrapancreatic infection
What are the arguments for and against the use of prophylactic antibiotics in this setting?
- High risk of infection (about 20% of the patients go on to develop necrosis, and about 8-12% of patients go on to develop infected necrosis (Mike Larvin, 2008)
- Organ system failure in these cases tends to be worse and mortality tends to be high
- Confirmation of the diagnosis is invasive, i.e. by samples and culture
- Penetration into the collection will be poor.
- Infection of the collection typically occurs after day 10; fever prior to this will usually be aseptic SIRS
- Organ system failure tends to be worse and mortality tends to be high
What is the evidence regarding the use of prophylactic antibiotics in pancreatitis?
- The most recent meta-analysis (Jafri et al, 2009) found no improvement in mortality, risk of pancreatic pseudocyst infection or need for surgical intervention. The risk of extrapancreatic infection, however, did improve (an absolute risk reduction of 15%, NNT =7).
- The Cochrane analysis referred to by the college in Question 1 from the first paper of 2016 is Villatoro et al (2010), whose conclusion was also "no benefit".
The patient undergoes an ERCP-guided aspiration of his abdominal collection. Culture comes back positive for Klebsiella oxytoca. What antibiotics will you choose?
- Drugs which achieve a high concentration in pancreatic tissue :
- Imipenem (and thus also meropenem)
- Fluoroquinolones (specifically, pefloxacin)
- Drugs which are known to penetrate poorly: