Failure to Awaken After Surgery


FIGURE 15.1 CT scan shows bilateral cerebellar hypodensities with acute obstructive hydrocephalus.



What do you do now?


Without doubt, abnormal wakefulness after a surgical procedure is the most common reason for neurological consultation in surgical intensive care units. The ambiguous- and unfortunately pervasive-term “altered mental status” is typically used to characterize patients who are not fully awake following a major surgical repair, and who do not respond well to the surgeon’s questions during rounds.


There are a few obvious causes. Complex cardiac or vascular procedures are most often associated with ischemic brain lesions. Most surgeons anticipate “trouble ahead” when mobile atherosclerotic plaques are found or prolonged hypotension has occurred during major vascular surgery, and both are strong indicators the brain could have been affected.


Ischemic stroke involving major arterial territories are expected in any type of vascular surgery, such as aortic arch replacement, surgery for aortic dissection, or any type of open-heart surgery. Strokes in the cerebellum can be explained by a vertebral occlusion (e.g., dissecting aorta occluding the vertebral artery origins), but the posterior circulation is often involved in cardiogenic stroke (postoperative myocardial infarction and new postoperative atrial fibrillation are known contenders). The diagnostic yield of MRI scan in a patient who remains stuporous can be substantial, and MRI can show multiple hemispheric lesions that may explain failure to awaken after anesthesia.


Multiple cases of postoperative stupor associated with bithalamic infarcts have been described. Therefore, MRI/MRA is essential in postoperative patients in whom sedation cannot explain the decreased level of consciousness.


In patients undergoing a general (nonvascular-noncardiac) surgical procedure—as in our case example—neurologic complications are not expected. Multiple ischemic strokes after a general surgical procedure (defined as urogenital, gastrointestinal, orthopedic, or chest surgery) without involving some sort of manipulation of vasculature is rare and hard to explain. It occurs most often in patients who have other stroke risk factors, such as peripheral vascular disease or ischemic cardiomyopathy. Hypotension does not play a major role unless an unexpected large blood loss has occurred. When ischemic stroke involves the posterior circulation resulting in cerebellar infarcts with obstructive hydrocephalus (explaining stupor), the diagnosis is difficult and often not recognized. This was clearly the case in our patient. Following any type of surgery, there is a tendency for strokes to occur in the posterior circulation territories, and therefore, it has been speculated that these strokes could be due to vertebral dissection occurring as a result of neck manipulation associated with anesthesia preparation. No such case has ever been documented to corroborate that explanation. In our patient example, the sudden appearance of a bilateral cerebellar infarct compressing the fourth ventricle led to an obstructive hydrocephalus. After ventriculostomy was placed, the patient improved substantially, and eventually the ventriculostomy was weaned and removed.


Finally, it is worth emphasizing that the cause of postoperative stupor in general surgical intensive care units usually is due to prolonged clearance of sedative drugs or excessive opioid use. The additional presence of multiorgan failure in critically ill patients may reduce clearance of any of these drugs, and a careful look at the medication dose, infusion rate, and expected clearance is necessary. Increased creatinine after cardiac surgery is a major determinant of prolonged awakening after cardiac surgery.


Also rare, but often considered a diagnostic possibility, is the presence of nonconvulsive status epilepticus. This is a highly unusual occurrence after any type of surgical procedure or in any critical illness. It can occur more often in patients who have had seizures or in patients who had a known seizure disorder and did not have their antiepileptic drugs administered.


Acute metabolic derangement such as acute hyponatremia or acute hyperglycemia are always considered and, occasionally, these derangements explain the clinical picture. In susceptible patients a surgical procedure may lead to an acute increase in serum ammonia (mostly young females in teenage years with an ornithine transcarbamylase deficiency or in patients after a lung transplantation).



TABLE 15.1 Causes to Consider in Patients Who Fail to Awaken after Surgery

























Excessive opioid use
Prolonged clearance of benzodiazepines with multiorgan failure
Postoperative stroke (hemisphere with mass effect)
Postoperative stroke (cerebellum with mass effect or hydrocephalus)
Postoperative PRES (aortic dissection repair)
Acute hyponatremia
Acute hypoglycemia or hyperglycemia
Acute hypercapnia with hypoxemia
Acute uremia
Acute increase in arterial ammonia
Nonconvulsive status epilepticus

PRES: Posterior reversible encephalopathy syndrome.

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Jan 31, 2018 | Posted by in NEUROSURGERY | Comments Off on Failure to Awaken After Surgery

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