- General approach to neuroworsening after cranial surgery
- General postoperative management considerations
- General complications
- Selected procedures
- Questions & discussion
approach to neuroworsening after cranial surgery
common causes of neurologic deterioration include:
- Cerebral edema.
- Intracranial hemorrhage.
- Acute ischemic stroke.
- Hyponatremia or hypoglycemia.
- Hypothermia (e.g., due to hypothalamic injury).
- Medication-induced delirium.
- Exacerbation of a pre-existing medical problem, for example:
- Hypercapnic encephalopathy in the context of baseline COPD or obesity hypoventilation syndrome (OHS).
- Alcohol withdrawal.
- Hepatic encephalopathy in the context of cirrhosis.
- Withdrawal of chronic medication therapy (e.g., Parkinson's medications).
- Diabetic ketoacidosis in the context of type I diabetes.
investigations to consider to evaluate neuroworsening:
- Evaluation of vital signs (hemodynamics, oxygen saturation, adequate respiratory efforts, temperature.)
- Neurological examination.
- Chart review, focusing on:
- Baseline medical problems.
- Home medication list.
- Current Medication Administration Record (MAR).
- STAT fingerstick glucose.
- Electrolytes, renal function, Ca/Mg/Phos.
- ABG/VBG if there is a clinical concern for hypercapnia (e.g., in a patient with chronic COPD or obesity hypoventilation).
- Cerebrospinal fluid analysis (either lumbar puncture or sampling fluid from a ventricular drain).
- Neuroimaging (often beginning with a CT scan +/- CT angiography or CT venography, depending on the level of concern for arterial or venous injury).
- Postoperative hypertension could increase the risk of intracranial hemorrhage and edema, so it should be avoided.
- Potential causes of hypertension may include:
- Undertreated pain or anxiety.
- Bladder distension.
- Rebound hypertension after holding home antihypertensives.
- Volume overload.
- Elevated intracranial pressure; for example, due to intracranial hemorrhage.
- 💡 An abrupt, refractory increase in blood pressure may indicate an intracranial process with mass effect, so imaging should be considered.(Wijdicks, 2019)
- Reflexive response to neurological injury (the body's efforts to perfuse an ischemic penumbra).
- Management should ideally focus on addressing the cause of the hypertension. For example:
- Restarting chronic antihypertensive medications.
- Treatment of pain and/or anxiety.
- Volume overload management with diuresis.
- If no immediately treatable cause is evident, hypertension should be controlled with an antihypertensive agent. For patients with labile hypertension, a titratable infusion (e.g., nicardipine) may be safer than a long-acting antihypertensive agent.
- Blood pressure targets may vary between patients, depending on their baseline blood pressure and details of the surgical procedure. The optimal blood pressure should ideally be clarified with the neurosurgical team. A target systolic pressure <150-160 mm may be reasonable for most patients.(Wijdicks, 2019; Webb, 2016)
- More on the management of hypertensive emergency & antihypertensive pharmacology here: 📖
- Hypotension is less common than hypertension.
- A general approach to shock is shown below.📖
- Causes of hypotension following neurosurgery include:
- Volume depletion (e.g., due to mannitol administration).
- Anaphylaxis due to medication or blood administration.
- Pulmonary embolism.
- Septic shock.
- Takotsubo cardiomyopathy.
- Bradycardia due to surgical stimulation of the vagal nucleus in the brainstem.(Shutter, 2019)
- Adrenal insufficiency (for patients on chronic steroid therapy, if this was held prior to surgery).
- Hypotension may threaten to cause malperfusion of injured brain tissue. Thus, immediate hemodynamic stabilization may be warranted (e.g., using norepinephrine) while simultaneously evaluating the etiology of the hypotension.
seizure prophylaxis & management
- This is controversial, with guidelines generally recommending against prophylaxis. In particular, prophylaxis is definitely unnecessary for surgery involving the posterior fossa.(Wijdicks, 2019)
- 💡 Seizures are not known to arise from posterior fossa structures.(Torbey, 2019)
- Many centers will use levetiracetam for one week following surgeries at higher risk of seizure (e.g., levetiracetam 500 mg BID for procedures involving the supratentorial cortex).
- Subdural hematoma evacuation carries an especially high risk of seizures, which often occur within the first few postoperative days.(34618765) (More on seizure prophylaxis following traumatic brain injury here.📖)
- Clinical manifestations may include eye deviation, eyelid fluttering, staring, or tonic-clonic movements.
- Nonconvulsive seizures may cause subtle involuntary movements, aphasia, fluctuating encephalopathy, or altered behavior.(34618765)
- In cases that aren't clear, diagnosis is based on continuous EEG.
more common causes of postoperative seizure include:
- Manipulation of brain tissue.
- Edema (including edema caused by venous sinus thrombosis).
- Acute ischemic stroke.
- Intracranial hemorrhage.
- Sodium abnormalities.
- Withdrawal from alcohol or benzodiazepines.
- Medication management issues:
- Medications that may reduce the seizure threshold.
- Epilepsy, with interruption of antiepileptic therapy due to surgery.
- (More complete list of the causes of seizure here: 📖)
investigation of the cause of a postoperative seizure
- 🚨 STAT fingerstick glucose.
- Electrolytes, including Ca/Mg/Phos.
- Antiepileptic drug levels, if relevant.
- Neuroimaging (generally beginning with a CT scan).
- Medication review for agents that promote seizure.
- EEG (may help clarify the diagnosis and monitor for seizure recurrence).
- (More extensive investigation into the causes of seizure here: 📖)
- (1) Seizure management:
- A self-limiting seizure may be managed with initiation or escalation of antiepileptic agents.
- Convulsive status epilepticus should be treated in the usual fashion.📖
- (2) Treatment of underlying causes:
- Investigation should be undertaken for all contributory factors (as listed above).
- All treatable factors that are contributing to the seizure should be managed.
analgesia & sedation
- Multimodal analgesia is beneficial, as for any critically ill patient.
- Most patients may benefit from scheduled acetaminophen 💉 (e.g., 1 gram q6hr).(Wijdicks 2019; Velly 2016).
- Nonsteroidal anti-inflammatory agents (NSAIDs) are generally avoided due to risks of acute kidney injury, gastrointestinal hemorrhage, or impaired platelet function promoting intracranial hemorrhage.(Kumar 2019)
- Intermittent doses of as-needed opioid are often required (table below). Patients who are awake and alert may benefit from patient-controlled analgesia (PCA).📖
- Unusual or refractory headache should raise concern for complications (e.g., CSF leak, meningitis, cerebral edema, hemorrhage).(34618765)
- More on analgesia for critically ill patients here: 📖.
- Longer-acting sedatives (e.g., benzodiazepines) should be avoided if possible, to allow lifting sedation for the purpose of neurological examinations. For intubated patients, a propofol or dexmedetomidine infusion are typically preferred options.
- More on sedation for critically ill patients here: 📖.
postoperative nausea & vomiting
- Usual treatments may include:
- Ondansetron 8 mg infused over 15 minutes (💡 the risk of torsade de pointes relates largely to rapid administration of ondansetron; this may be minimized by gradual infusion).
- Promethazine 10 mg IV q6-8 hours.
- Droperidol or haloperidol (doses shown in the table above).
- Intractable nausea/vomiting may reflect elevated intracranial pressure, which may require further evaluation.
- More on the management of nausea/vomiting here.📖
- Hyponatremia is common following craniotomy, occurring in about half of patients.
- Rapid drops in sodium concentration may cause delirium, seizures, and cerebral edema. Thus, moderate hyponatremia or rapid declines in serum sodium require active management.
- The most common causes of hyponatremia following neurosurgery include SIADH (syndrome of inappropriate antidiuretic hormone secretion) and cerebral salt wasting. These can be very difficult to differentiate from one another. The initial therapeutic strategy for both is largely identical (with hypertonic saline used to increase the sodium). Patients with ongoing volume losses due to cerebral salt wasting may additionally benefit from fludrocortisone, to reduce ongoing fluid losses.
- Surgery near the pituitary may cause adrenal insufficiency (causing hyponatremia).
- The approach to hyponatremia following neurosurgery is very similar to the approach to hyponatremia in patients with subarachnoid hemorrhage, which is discussed further here.📖
- For patients with numerous medical comorbidities (e.g., cirrhosis, heart failure), a broader approach to hyponatremia may be appropriate. The general approach to hyponatremia is explored further here.📖
- ⚠️ Note that changes in serum sodium are generally more important than the absolute sodium value. Additionally, rapid increases in sodium (>8 mM/day) may cause a risk of osmotic demyelination. Thus, if a patient is chronically hyponatremic, rapidly increasing their sodium to a normal or elevated level may be unsafe.
- Common causes of hypernatremia include the following:
- Mannitol administration, or excessive administration of hypertonic saline.
- Inadequate administration of free water, causing gradual hypernatremia over several days (this is frequently encountered among patients who are intubated or NPO).
- Central diabetes insipidus (e.g., following pituitary surgery or severe traumatic brain injury).
- Hypernatremia should be treated promptly, as it may promote delirium and agitation (due to profound thirst).
- Among conscious patients who are able to drink, free access to drinking water will often reverse hypernatremia. Otherwise, the free water deficit must be calculated and provided either enterally or intravenously (as D5W).
- Patients with central diabetes insipidus will require titrated doses of desmopressin (DDAVP) combined with free water. This must be done very carefully, to avoid overshooting and causing hyponatremia. Management of diabetes insipidus is discussed further below.📖
- The chapter on hypernatremia is here: 📖
- Sequential compression devices should be utilized if the patient is unable to receive chemical DVT prophylaxis (e.g., in the immediate postoperative period).
- DVT prophylaxis can often be started within 24-48 hours postoperatively, in the absence of hemorrhagic complications.
- Unfractionated heparin might be preferred over low molecular-weight heparin in the early postoperative period, as this may be stopped or reversed more easily.
- Timing of DVT prophylaxis should be discussed with the neurosurgical team.
- Hemorrhage may occur at various locations (e.g., intraparenchymal, subarachnoid, subdural, epidural). Hemorrhage is usually near the operative bed, but it may occasionally develop at sites remote from the surgery (usually the cerebellum).(26426239)
- Hemorrhage often occurs within six hours of surgery, but it may also occur as a delayed complication emerging within the first few postoperative days.(Nanda 2019)
- Potential causes include:
- Surgical trauma.
- Residual tumor.
- Hemorrhagic transformation of an ischemic infarction.
- Hypertensive surges during recovery.(26426239)
- Remote site hemorrhage may result from sudden decompression of elevated intracranial pressure or excessive CSF loss, causing brain sagging that compresses draining veins.(34618765)
presentation may include
- Deterioration in level of consciousness.
- Focal deficit or worsening of pre-existing deficit.
- Worsening headache.
- New-onset hypertension.
- CT head.
- Note that a small, 1-3 mm hematoma in the subdural or subgaleal space may be a normal postoperative finding.(30255407)
- Evaluation of coagulation studies (complete blood count, INR, PTT, fibrinogen level).
- Aggressive reversal of any coagulopathy.📖
- Control SBP to <140-160 mm.
- Intraoperative subarachnoid hemorrhage may lead to delayed cerebral edema (similar to a spontaneous subarachnoid hemorrhage), so this may merit monitoring. More on delayed cerebral edema here.📖
- Surgical evacuation may be necessary.
causes of cerebral infarction may include:
- Cessation of anticoagulation prior to the procedure, or anticoagulation reversal.
- Direct vessel injury to arteries or veins.
- Coil dislodgement causing arterial occlusion.
- Vasospasm (due to vessel traction or exposure to cisternal blood, often following surgery for a tumor within the sellar region).
- Delayed cerebral edema may complicate basal cisternal blood from an intraoperative subarachnoid hemorrhage, similar to that seen in spontaneous aneurysmal subarachnoid hemorrhage.(34618765) This may occur days or even weeks after the procedure.(26426239) Treatment may be similar to treatment of vasospasm following subarachnoid hemorrhage, although prior radiotherapy may increase the risk of hemorrhage due to blood pressure augmentation.📖
- Cerebral air embolism (may occur in patients with right-to-left shunt who undergo surgery in a sitting position).
- Thrombolysis is contraindicated in the postoperative period. However, mechanical thrombectomy may be an option for large vessel occlusions.
- Usually permissive hypertension is allowed in acute ischemic stroke, to encourage perfusion of the ischemic penumbra. However, hypertension may increase the risk of hematoma formation following neurosurgery. A reasonable blood pressure target might be a systolic blood pressure <160 mm.(Kumar 2018)
- More on the management of acute ischemic stroke here: 📖
causes of brain edema
- Intraoperative retraction of brain tissue (edema often peaks 48-72 hours postoperatively).
- Injury to the venous system:
- Sacrifice of veins during surgery.
- Cerebral venous thrombosis may occur, whether or not the cerebral venous sinuses were manipulated.(26426239) This may emerge as a delayed complication.
- Partial resection of a tumor, especially glioblastoma (with irritation of surrounding tissue that is infiltrated by tumor cells).
presentation may include
- Focal edema may cause a focal deficit, or worsening of a pre-existing deficit.
- Global edema may rarely manifest as reduced consciousness.(34618765)
- Rarely, edema may cause herniation.📖
- CT head (+/- CT venogram to evaluate for venous sinus thrombosis).
- In mild cases, observation may be sufficient (e.g., lack of substantial mass effect or reduced level of consciousness).(26426239)
- In moderate/severe injury, treatment for cerebral edema may be needed:
- Osmotherapy may be considered.
- Steroid may be considered for patients with vasogenic edema producing mass effect. For example, edema surrounding a brain tumor may be managed with dexamethasone 10 mg followed by 4-6 mg q6hr.(Torbey, 2019)
- More on the management of elevated intracranial pressure here.📖
- For patients with edema due to cerebral venous thrombosis, anticoagulation may be considered.📖
- Surgeries with especially highest risk of CSF leak:
- Posterior fossa surgery carries a 3-12% risk of CSF leak.(26426239) These surgeries often involve leaving part of the skull removed (craniectomy rather than craniotomy). Dural defects may not be covered postoperatively with bone, so a CSF fistula may form even with immaculate dural closure.(Torbey, 2019) This often leads to a suboccipital CSF fluid collection (pseudomeningocele; see figure below).
- Transsphenoidal pituitary surgery carries a ~10% risk of CSF leak.(34618765)
- The relationship between CSF leak and infection is bidirectional:
- CSF leak is a risk factor for meningitis, empyema, or brain abscess.
- Wound infection may occasionally cause a CSF leak.(Nanda 2019)
- CSF leakage:
- Drainage of CSF from the ear or nose (CSF rhinorrhea).
- Drainage of CSF from the incision.
- Growth of a fluctuant fluid collection (pseudomeningocele 🌊). Persistent increases in the fluid collection over time raise suspicion for a CSF leak.
- Symptoms of intracranial hypotension:
- Headache that is worse when sitting up.
- Visual symptoms, impaired mental status.(Kumar 2018)
- If there is doubt about whether fluid is originating from the CSF, beta-2-transferrin levels in the fluid may be measured.(26426239)
- Evaluate for hydrocephalus (which might be causing the CSF leak).
- Evaluate for pneumocephalus (which might be a result of intracranial hypotension due to a CSF leak). More on pneumocephalus here.📖
- MRI is more sensitive than CT for intracranial hypotension. Findings may include:(Kumar 2018)
- Widened extra-axial fluid spaces without focal extra-axial fluid collection
- Dural thickening and enhancement of the meninges.
- Many CSF leaks will improve following conservative therapy (e.g., elevating the head of the bed).(34618765)
- Minor pseudomeningoceles may be followed without aggressive interventions.(Albin 2022)
- IV antibiotics to prevent meningitis may be considered, especially for CSF leaks opening into the nasopharynx.
- A lumbar drain to divert CSF may reduce intracranial pressure, facilitating healing of the CSF leak.(34618765)
- Re-exploration of the wound may be needed, especially if a pseudomeningocele has formed.
causes of hydrocephalus include:
- Hydrocephalus may result from obstruction of the normal channels for CSF drainage. This is especially likely if surgery occurs nearby (e.g., posterior fossa surgery may cause edema or clots which obstruct the fourth ventricle).
- Hemorrhage into the ventricular system may cause hydrocephalus.
- Decompressive craniectomy (with damage to the superior sagittal sinus).
presentation may include: (Kumar 2018)
- Features of elevated intracranial pressure:
- Headache which is worse when lying down, and which may be accompanied by nausea/vomiting.
- Blurred or double vision (due to abducens nerve palsy).
- Lethargy, irritability, or reduced level of consciousness.
- Upgaze limitation causing “sun setting” of the eyes.
- Urinary incontinence and gait difficulty (if the patient is ambulatory).
- Hydrocephalus may promote a secondary CSF leak and/or pseudomeningocele (collection of CSF under the scalp).
- CT head.
- CSF diversion with external ventricular drain is often needed for acute hydrocephalus.
- If marked edema or bleeding in the posterior fossa causes hydrocephalus, simultaneous surgical decompression may be needed. In this situation, solely placing an external ventricular drain could cause upwards herniation of the midbrain.
fever & infectious complications
differential diagnosis of fever after neurosurgery
- Noninfectious causes:
- Benign postoperative fever (postoperative day #1-3; usually <39C/102F).
- Febrile transfusion reaction (within 6 hours of transfusion).
- Drug fever.📖
- Medication-induced hyperthermia (serotonin syndrome 📖, neuroleptic malignant syndrome 📖, malignant hyperthermia 📖).
- Pulmonary embolism (usually low-grade fever, <39/102).(10631196)
- Neurogenic fever.📖
- Infection at remote sites:
- Infectious causes related to neurosurgery:
- Superficial surgical site infection (e.g., cellulitis, subcutaneous abscess).
- Cranial osteomyelitis.
- Meningitis (occurs in ~0.6% of neurosurgical procedures).(Nanda 2019)
- Subdural empyema 📖, epidural empyema 📖.
- Brain abscess.📖
- Hardware infection (e.g., ventriculitis due to an external ventricular drain 📖).
evaluation of fever: tests to consider
- Physical examination, focusing on:
- Wound appearance.
- Ventilator settings and sputum production.
- Sites of any lines or drains.
- Evidence of deep vein thrombosis.
- Chest X-ray for patients who are intubated or have signs/symptoms of pulmonary dysfunction.
- Blood cultures.
- Sputum culture, only if ventilator-associated pneumonia is clinically suspected.
- CT head.
- Lumbar puncture (if meningitis is suspected) or CSF sampling from an external ventricular drain (EVD). However, postoperative meningitis cannot be diagnosed based on CSF leukocyte count following surgery.(Velly 2016; Torbey, 2019) Low glucose or elevated lactate may be more helpful, similar to ventriculitis in the context of an external ventricular drain.📖
- Aseptic meningitis: Implantation of prosthetic material (e.g., a dural graft) may cause sterile inflammation of the meninges, leading to pleocytosis and low CSF glucose.(26426239)
- Evaluation for PE/DVT may be considered (e.g., leg ultrasonography +/- CT angiography).
management of fever
- Maintenance of normothermia is generally desirable for patients with acute brain injury, including post-neurosurgical patients.
- Acetaminophen may be both therapeutically and diagnostically helpful. Failure of the fever to respond to acetaminophen suggests that the fever is not mediated in the normal fashion by prostaglandins in the hypothalamus (e.g., this may suggest a central fever).
management of surgical site infection
- This will vary depending on the anatomic site of infection, but some general themes are usually:
- Exploration and debridement may be needed.
- Removal of any infected hardware or drains (which may require insertion of a new, sterile drain).
- IV antibiotics with appropriate coverage (e.g., cefepime/meropenem plus vancomycin). However, in stable patients who are soon to have surgical drainage (e.g., for an abscess), temporarily withholding antibiotics may be reasonable pending collection of cultures.
- The general approach to fever in the ICU: 📖
- Brain abscess: 📖
- Intracranial epidural abscess: 📖
- Subdural empyema: 📖
- Ventriculitis due to an external ventricular drain (EVD): 📖
- Tension pneumocephalus usually results from a CSF leak with a ball-valve effect that allows the entry of air, but prevents the exit of air. Risk factors for this include the following: (Velly, 2016)
- Intraoperative mannitol use.
- Surgery in a sitting position.
- Ventriculoperitoneal shunt.
- Nitrous oxide anesthesia.
- Overdrainage from a lumbar drain.(30761443)
- Tension pneumocephalus may occur following neurosurgery, or from other causes of a CSF leak (e.g., trauma or a spontaneous CSF leak).
- Signs of elevated intracranial pressure (e.g., headache, nausea/vomiting, altered consciousness).
- Seizures may occur.
- Focal neurologic deficits.
CT scan findings
- Small amounts of subdural air may normally occur following craniotomy, especially along the frontal lobes. This may take up to three weeks to resorb.(34618765) The amount of air should remain stable or decrease between interval scans, rather than increase.
- Pathological findings that suggest tension pneumocephalus:
- (1) Large amounts of air in the subdural space separating the frontal lobes, creating the Mount Fuji sign. However, this sign can occur in asymptomatic patients, so it's not pathognomonic for symptomatic tension pneumocephalus.(30761443)
- (2) Multiple small air bubbles scattered through several cisterns (“air bubble sign”).
- Differential diagnosis:
- Infection with gas-producing anaerobes.
- CSF leak may cause a persistent pneumocephalus (without tension).(30761443)
- Supplemental 100% oxygen may accelerate reabsorption of gas (e.g., 100% nonrebreather mask with a nasal cannula at 15 liters/minute underneath it).
- For tension pneumocephalus, neurosurgical management is needed (e.g., frontal burr hole).
potential complications after decompressive craniectomy
- Acute postoperative hematoma (may be subgaleal, epidural, or subdural) or subdural/subgaleal effusion. These may compress the underlying brain tissue, thereby negating the benefit of the decompressive craniectomy (figure above).
- 💡 Development of a tense skin flap may signal a postoperative hematoma.
- Expansion of hemorrhagic contusions (in patients with traumatic brain injury).
- Brain herniation through the bone defect.
- Seizures (may reflect intracranial pathology, such as postoperative hemorrhage, infection, or edema).(Nanda 2019)
- Hydrocephalus (may result from disruption of the superior sagittal sinus).
- Infection (e.g., meningitis, ventriculitis, wound infection).
- Sinking skin flap syndrome, paradoxical herniation (more on these below).
sinking skin flap syndrome (aka, syndrome of the trephined)
- Atmospheric pressure, as well as a lack of support by the skull, causes brain tissue underneath the skin flap to sink downwards, potentially even leading to herniation.
- This usually occurs several months postoperatively.
- Symptoms may include headache, dizziness, altered level of consciousness, seizures, and focal neurological deficits (e.g., hemiparesis, aphasia).
- Management requires cranioplasty. Unfortunately, cranioplasty itself may cause additional complications (e.g., seizures, subgaleal collections, hydrocephalus, bone flap infection, rebound overperfusion of the underlying brain tissue).(34618765)
- This refers to downward herniation that occurs despite craniectomy (this is termed “paradoxical” because the brain herniates downwards instead of swelling outwards – as it's supposed to, after craniectomy). The physiology has some similarities to sinking skin syndrome, with paradoxical herniation promoted by an imbalance between atmospheric pressure (pushing the brain downwards) versus CSF pressure (pushing the brain upwards).
- Paradoxical herniation may occur at any time following craniectomy.(Kumar 2018) It may be precipitated by CSF drainage (e.g., by lumbar puncture, lumbar drain, ventricular drain, or development of a CSF leak).(Nanda 2019)
- Symptoms may include reduced level of consciousness, pupillary changes, focal neurologic deficits, and autonomic instability.(Kumar 2018)
- Management of acute paradoxical herniation:
- Lower the head of the bed.
- Discontinue any diversion of CSF (e.g., clamp a lumbar drain).
- Discontinue hyperosmotic agents (these may exacerbate herniation).
- Once the acute crisis has been managed, cranioplasty may prevent recurrence.
posterior fossa surgery
The amount of space in the posterior fossa is small. Bleeding or edema within the posterior fossa may rapidly compress the adjacent brainstem or the fourth ventricle (causing obstructive hydrocephalus) – creating an immediate neurological emergency.
cranial nerve injuries
- Injury to CN5 or CN7 may lead to failure to protect the cornea. Care should be taken to provide adequate eye care (e.g., eye drops, taping the eyelid shut at night).
- Injury to lower cranial nerves may impair coughing and swallowing. Caution should be undertaken when extubating patients and advancing their diet.
obstructive hydrocephalus – more on this above 📖
CSF fistula – more on this above 📖
surgery for pituitary tumor
Pituitary surgery is perhaps most notable for various endocrine complications which commonly occur. In the immediate postoperative period, adrenal dysfunction and sodium abnormalities are the predominant concerns. Other problems (e.g., hypothyroidism) may manifest later on.
- Hydrocortisone is often initiated prophylactically in the postoperative period (e.g., 50 mg IV q6hr). This may be tapered off subsequently, with monitoring of AM cortisol levels to ensure adequate adrenal function:(Kumar 2018)
- AM cortisol level is normally ~5-23 mcg/dL (or 138-635 nM)
- AM cortisol level >16 ug/dL (>450 nM) suggests adequate adrenal function.
- AM cortisol level <4 ug/dL (<100 nM) strongly suggests adrenal insufficiency in this context.
- If hydrocortisone is not started empirically, patients should be monitored closely for the development of adrenal insufficiency (e.g., monitoring of AM cortisol levels and hemodynamics, with any hemodynamic instability raising concern for adrenal insufficiency).
- More on the diagnosis of adrenal insufficiency here.📖
diabetes insipidus (causing hypernatremia)
- This is a common complication, affecting ~25% of patients postoperatively.(Kumar 2018) Diabetes insipidus may begin 24-48 hours after surgery, so ongoing vigilance is required.
- If the urine output is >250 ml/hour or the patient is becoming hypernatremic, this should immediately raise concern for the possibility of diabetes insipidus.
- Diabetes insipidus is diagnosed based on a combination of three features:
- Elevated urine output.
- Persistently dilute urine (e.g., specific gravity <1.005 or urine osmolality <200 mOsm).
- Serum sodium >145 mM.
- Differential diagnostic possibilities include: (26426239)
- Mannitol administration.
- Excretion of excess fluid administered during surgery.
- Diuresis due to hyperglycemia (i.e., glucosuria).
- Meticulous monitoring of sodium is important, as excessive reduction could promote cerebral edema. In general, two strategies are possible:
- Rx option #1: For a conscious patient who is able to drink, the patient may be instructed to drink as much water as is needed to satisfy their thirst. In the absence of concomitant hypothalamic injury, a conscious person should be able to match their water losses and maintain eunatremia. For an awake patient, drinking ad libitum is the most comfortable therapy.
- Rx option #2: For patients who are altered or NPO, vasopressin should be replaced (e.g., desmopressin 2 mcg IV q8hrs, or 10 mcg intranasal BID). This may be a supraphysiologic dose of desmopressin, so it can cause patients to retain free water. To avoid hyponatremia, free water intake must be restricted. Likewise, large volumes of fluid administration should be avoided, as they will tend to cause hyponatremia. (This is fundamentally a variation of the DDAVP clamp strategy 🌊.)
- (Note: Other treatment strategies are possible, including timing/titrating DDAVP doses based on urine output. These strategies can be a bit complex, so they might ideally be restricted to units/clinicians which are experienced in their use. If in doubt, consult nephrology.)
SIADH (causing hyponatremia)
- Damage to the pituitary gland may rarely cause a transient release of antidiuretic hormone, leading to the syndrome of inappropriate ADH secretion (SIADH). This is often followed by the development of diabetes insipidus.
visual deterioration and/or ophthalmoplegia
- Differential diagnosis includes:
- Damage to the optic nerves.
- Suprasellar hematoma formation.
- Herniation of the chiasm into the empty sella.
- Injury to cranial nerves III, IV, and VI (this usually improves over time, but the possibility of a carotid-cavernous sinus fistula may also be considered).
- Investigation involves a CT scan with CT angiography (to identify a carotid pseudoaneurysm or carotid-cavernous fistula).
- Hematoma formation or herniation of the chiasm may require re-operation.
complications from the transsphenoidal approach (which is most commonly utilized)
- (1) CSF leak and CSF rhinorrhea is discussed above.📖
- (2) Meningitis may occur, especially if there is sphenoid sinusitis at the time of surgery.(30761443)
- ⚠️ Noninvasive positive pressure ventilation is contraindicated (e.g., CPAP or BiPAP).(Albin 2022)
carotid endarterectomy or stenting
- (1) Hypotension due to autonomic shifts:
- This may result from intraoperative baroreceptor blockade, exposure of the carotid receptor to markedly increased postoperative blood flow, or vagus nerve dysfunction.(Torbey 2019)
- Hypotension generally responds well to fluid and vasopressors (e.g., phenylephrine infusion). Blood pressure lability is common during the first postoperative day, so ongoing titration may be needed.
- Hypotension usually lasts only 24-48 hours.(Kumar 2018)
- (2) Other causes of hypotension:
- The differential diagnosis of hypotension is broad (more on this above 📖).
- Other causes of hypotension should especially be considered if hypotension is refractory to basic interventions, or if it persists >48 hours.
- Patients undergoing carotid endarterectomy have a substantial burden of atherosclerotic vascular disease, so they have a relatively high rate of postoperative myocardial infarction. There should be a low threshold to obtain an EKG and bedside echocardiography.
- Causes of postoperative hypertension are discussed above 📖. In addition to the usual causes, some patients may develop baroreflex failure syndrome if there is damage to the bilateral carotid baroreceptors. This usually resolves within 1-2 days, but it can persist for up to 12 weeks.(Kumar 2018)
- ⚠️ Adequate control of hypertension is essential, as this may be the single most important modifiable factor to reduce periprocedural morbidity after carotid endarterectomy.(Kumar 2018)
- Management of hypertension may reduce the risk of cerebral hyperperfusion syndrome (discussed below).
- Patients may have labile blood pressure, so an antihypertensive infusion may be helpful (e.g., nicardipine).
- The optimal blood pressure target is unclear, and may vary depending on the patient's baseline pressures. Targeting a systolic blood pressure of 110-150 mm may be reasonable for most patients.(Kumar 2018)
cerebral hyperperfusion syndrome (~2% incidence)
- Chronic hypoperfusion leads to a loss of autoregulation in the arterial system distal to the carotid stenosis. Restoration of blood flow postoperatively then leads to a hyperemic state, with some similarities to posterior reversible encephalopathy syndrome (PRES).(Torbey 2019)
- Symptoms of cerebral hyperperfusion may include headache, nausea/vomiting, or focal deficits (e.g., hemiparesis and dysphasia).
- Cerebral hyperperfusion syndrome seems to be a leading cause of seizures or intracerebral hemorrhage after carotid endarterectomy.
- Hypertension increases the risk of cerebral hyperperfusion syndrome, so if present this should also heighten suspicion.
- Neuroimaging to evaluate for hemorrhage or ischemic stroke.
- Transcranial doppler of the middle cerebral artery may confirm the diagnosis, based on a 100% increase in cerebral perfusion to above the preoperative level.
- Treatment involves careful reduction of the blood pressure, while avoiding hypotension (e.g., using a nicardipine infusion).
ischemic stroke (~3% incidence)
- Causes include embolic stroke, carotid occlusion, or carotid dissection.
- Investigation may include CT angiography +/- CT perfusion scan (and perhaps Doppler ultrasonography of the carotid).
- If the internal carotid artery is occluded, surgical re-exploration may be indicated.
cranial nerve injuries
- Cranial nerves 9-12 lie adjacent to the carotid artery. Some cranial nerve palsies commonly occur due to traction during surgery, often resolving spontaneously:(Torbey 2019)
- Injury of the marginal mandibular branch of the facial nerve due to pressure from retraction may cause isolated mouth asymmetry.(CN7) This may mimic stroke, but it is limited to the mouth muscles and weakness is ipsilateral to the surgical site.(Nanda 2019)
- Glossopharyngeal nerve injury may affect carotid sinus innervation, leading to bradycardia or hypotension. (CN9)(26426239)
- Vagus nerve injury may cause reduced coughing or hoarseness. (CN10)(26426239)
- Spinal accessory nerve injury may cause shoulder weakness or pain. (CN11).
- Hypoglossal nerve injury may cause tongue deviation and dysarthria. (CN12)
- Horner's syndrome may result from injury to sympathetic fibers surrounding the carotid.
- Other cranial nerve abnormalities are more worrisome:
- Pupillary asymmetry with unilateral blindness suggests embolization of the ophthalmic artery.
- Wound hematoma may compress the airway. Management involves securing the airway, followed by surgical re-exploration. Intubation may be safer if performed early, before the hematoma is allowed to expand further. However, with advanced hematomas intubation may be anatomically challenging – so strategies such as awake fiberoptic intubation may be helpful. If the airway is already substantially distorted, opening the incision with or without drainage of the hematoma may be performed prior to intubation (ideally in the operating room).
- 🚨 Wound hematoma is potentially a combined airway & neurosurgical emergency. This may be ideally treated in the operating room, involving simultaneous management by anesthesiology and neurosurgery.
- Signs of wound hematoma may include:
- Increasing neck circumference.
- Tracheal deviation.
- 💡Wound hematoma should always be considered early in a patient with postoperative respiratory distress following carotid endarterectomy.
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questions & discussion
To keep this page small and fast, questions & discussion about this post can be found on another page here.
- Maintain a broad differential diagnosis for common presentations (e.g., fever), as the range of potential causes is often very broad.
- Neuroworsening should be aggressively investigated (generally including neuroimaging), to allow for early detection of complications.
Guide to emoji hyperlinks
- = Link to online calculator.
- = Link to Medscape monograph about a drug.
- = Link to IBCC section about a drug.
- = Link to IBCC section covering that topic.
- = Link to FOAMed site with related information.
- 📄 = Link to open-access journal article.
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- 26426239 Fugate JE. Complications of Neurosurgery. Continuum (Minneap Minn). 2015 Oct;21(5 Neurocritical Care):1425-44. doi: 10.1212/CON.0000000000000227 [PubMed]
- Velly, L., Simeone, P., & Bruder, N. (2016). Postoperative Care of Neurosurgical Patients. Current Anesthesiology Reports, 6(3), 257–266. https://doi.org/10.1007/s40140-016-0175-4
- Webb, A., Angus, D., Finfer, S., Gattioni, L., & Singer, M. (2016). Oxford Textbook of Critical Care (2nd ed.). Oxford University Press.
- Kumar, M., Levine, J. M., Kofke, W. A., & Schuster, J. (2018). Neurocritical Care Management of the Neurosurgical Patient (1st ed.). Elsevier.
- 30255407 Chughtai KA, Nemer OP, Kessler AT, Bhatt AA. Post-operative complications of craniotomy and craniectomy. Emerg Radiol. 2019 Feb;26(1):99-107. doi: 10.1007/s10140-018-1647-2 [PubMed]
- 30761443 Haber MA, Abd-El-Barr M, Gormley W, Mukundan S, Sodickson AD, Potter CA. Neurosurgical complications: what the radiologist needs to know. Emerg Radiol. 2019 Jun;26(3):331-340. doi: 10.1007/s10140-019-01672-5 [PubMed]
- Shutter, L. A., Molyneaux, B. J. (2019). Neurocritical care. Oxford University press.
- Torbey, M. T. (2019). Neurocritical Care (2nd ed.). Cambridge University Press.
- Wijdicks E.F.M., Findlay, J. Y., Freeman, W. D., Sen A. (2019). Mayo Clinic critical and Neurocritical Care Board Review. Oxford University Press.
- Nanda, A. (2019). Complications in Neurosurgery (1st ed.). Elsevier.
- 34618765 Sarwal A. Neurologic Complications in the Postoperative Neurosurgery Patient. Continuum (Minneap Minn). 2021 Oct 1;27(5):1382-1404. doi: 10.1212/CON.0000000000001039 [PubMed]
- Albin, C. S. W., & Zafar, S. F. (2022). The Acute Neurology Survival Guide: A Practical Resource for Inpatient and ICU Neurology (1st ed. 2022 ed.). Springer.