A previously fit and well 24 year old man sustained an isolated C5-C6 spinal injury following  a  diving  accident  resulting  in  a  tetraplegia.  The  spinal  fracture  was surgically fixed the following day and the patient was extubated on Day 6 of his ICU admission. Within 4 hours of extubation, the patient developed respiratory distress requiring urgent rapid sequence induction and reintubation. The patient sustained a cardiac arrest soon after intubation.

List three (3) metabolic and three (3) gastrointestinal complications seen after spinal cord transection.

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College Answer

Metabolic 
Hyponatremia (SIADH)
Immobilisation hypercalcemia and nitrogen wasting

Hypothermia

GI 
Ileus 
acute gastric dilatation

stress ulcerations

Discussion

This question only has room enough for a few minutes of thought. It is, after all, only the third part of a multi-part question. And one could spend an excessively long time discussing the various physiological disturbances which occur in response to spinal cord injury.

Metabolic

Hyponatremia (SIADH) - due to spinal hypotension
Immobilisation hypercalcemia - due to mysterious mechanisms, likely associted with the loss of mechanical loading of bones (which is normally a trophic stimulus)

Nitrogen wasting - Again, the loss of trophic stimulus results in muscle wasting and increased protein catabolism .

Hypothermia - largely due to the loss of sympathetic control (i.e. the inability to correctly specify when one's cutaneous vessels dilate or constrict).

The original version of this question for some reason had "nitrogen wasting hypothermia" as a college answer, but as a kind reader has pointed out the college never had this weird combination of words in their paper. It makes no sense, and it seems nowhere else in the world do these words occur in this exact combination. (if you google it, the only answers you get are from sites which directly quote the CICM paper).

Gastrointestinal

Ileus due to loss of autonomic control.
Acute gastric dilatation due to the "body cast syndrome", compression of the duodenum between the aorta and the superior mesentric artery.

Stress ulcerations due to unopposed vagal stimulus of the acid-secreting parietal cells.

Physiological consequences of spinal cord transection are discussed in detail elsewhere.

References

References

 

Claus-Walker, J., and L. S. Halstead. "Metabolic and endocrine changes in spinal cord injury: I. The nervous system before and after transection of the spinal cord." Archives of physical medicine and rehabilitation 62.12 (1981): 595-601.

 

Claus-Walker, J., and L. S. Halstead. "Metabolic and endocrine changes in spinal cord injury: II (section 1). Consequences of partial decentralization of the autonomic nervous system." Archives of physical medicine and rehabilitation63.11 (1982): 569-575.

 

Claus-Walker, J., and L. S. Halstead. "Metabolic and endocrine changes in spinal cord injury: II (section 2). Partial decentralization of the autonomic nervous system." Archives of physical medicine and rehabilitation 63.11 (1982): 576-580.

 

Claus-Walker, J., and L. S. Halstead. "Metabolic and endocrine changes in spinal cord injury: III. Less quanta of sensory input plus bedrest and illness."Archives of physical medicine and rehabilitation 63.12 (1982): 628-631.

 

Claus-Walker, J., and L. S. Halstead. "Metabolic and endocrine changes in spinal cord injury: IV. Compounded neurologic dysfunctions." Archives of physical medicine and rehabilitation 63.12 (1982): 632-638.

 

GORE, RICHARD M., RICHARD A. MINTZER, and LEONID CALENOFF. "Gastrointestinal complications of spinal cord injury." Spine 6.6 (1981): 538-544.

 

Ebert, Ellen. "Gastrointestinal involvement in spinal cord injury: a clinical perspective." Journal of Gastrointestinal & Liver Diseases 21.1 (2012).

 

Lin, Vernon W., et al. "Temperature Regulation in Spinal Cord Disease." (2003). Spinal Cord Medicine: Principles and Practice. Demos Medical Publishing, Inc.