Complications in the Postanesthesia Care Unit

Free H₂O deficit (L) = (serum Na − 140) × body weight (kg) × 0.6/140

If fluid is replaced early, it is not necessary to administer free water (D₅W). Rather, a hypotonic solution such as 0.45% sodium chloride (NaCl) or lactated Ringer’s may be given. Insulin and potassium supplementation might be required when dextrose-containing fluids are used, especially if corticosteroids are administered concomitantly. When hormonal replacement is required, 1-deamino-8-d-arginine vasopressin (DDAVP), a synthetic analog of the natural hormone arginine vasopressin, can be given intravenously, subcutaneously, orally, or intranasally. The latter might not be feasible after transnasal trans-sphenoidal pituitary surgery. The usual intravenous or subcutaneous dose is 0.3 mcg/kg/day in two divided doses. The dose of oral medication is 0.05 to 1.2 mg/day at once or divided into two or three doses. The intranasal dose is 10 to 40 mcg/day in one to three doses. The dose is adjusted according to the patient’s sleep pattern and water turnover. Once intravascular volume has been restored, persistent hypernatremia may be treated with thiazide diuretics, such as hydrochlorothiazide, 50 to 100 mg/day intravenously.

B. Rhinorrhea of CSF may develop after transnasal trans-sphenoidal operations. Spontaneous resolution occurs commonly and clinical observation is sufficient in most cases. If signs of infection develop, antibiotic therapy and surgical repair are indicated.

C. Airway obstruction from bleeding and accumulation of blood and secretions in the pharynx sometimes occurs after transnasal trans-sphenoidal procedures. Frequent assessment of the patency of the airway and adequacy of ventilation is mandatory. Excessive bleeding might require tracheal reintubation and surgical consultation.

D. PONV might develop due to intraoperative swallowing of blood during trans-sphenoidal resection of pituitary tumors. To minimize the risk of PONV, the pharynx and stomach are suctioned at the conclusion of surgery and 5HT-3 receptor antagonists are administered prophylactically. Drugs include dolasetron, 12.5 mg in adults and 0.35 mg/kg intravenously in children, ondansetron, 4 mg over 4 minute for adults and children weighing > 40 kg and 0.1 mg/kg over 4 minute for children weighing < 40 kg, and granisetron, 0.1 to 1 mg intravenously. The reported incidence of PONV varies from 7.5% to 80%, and the effectiveness of prophylaxis against PONV varies from nil to 30 to 40%.

IV. COMPLICATIONS AFTER OPERATION FOR HEAD TRAUMA

Systemic sequelae of head trauma frequently become apparent in the postoperative period. These include adult respiratory distress syndrome, neurogenic pulmonary edema (NPE), cardiac arrhythmias, electrocardiographic (ECG) changes, disseminated intravascular coagulation, DI, syndrome of inappropriate antidiuretic hormone secretion (SIADH), hyperglycemia, hyperosmolar non-ketotic (HONK) hyperglycemic coma, and gastrointestinal ulcers and hemorrhage.

A. Neurogenic pulmonary edema (NPE) is a fulminant form of pulmonary edema, which can progress rapidly (within hours to days) toward either resolution or death. The pathologic characteristics of NPE are marked pulmonary vascular congestion, pulmonary arteriolar wall rupture, protein-rich edema fluid, and intra-alveolar hemorrhage. The etiology of NPE is a massive transient central sympathetic discharge from an increase in ICP and is particularly associated with hypothalamic lesions. The pathophysiology includes systemic vasoconstriction and left ventricular failure, redistribution of blood from the systemic to the pulmonary vessels, pulmonary venous constriction, and increased pulmonary capillary permeability. Treatment is aimed at reducing ICP, reducing sympathetic hyperactivity, mainly with alpha-adrenergic blockers such as diazoxide, 1 to 3 mg/kg intravenously every 5 minute, until BP is controlled, up to 150 mg, or phentolamine in 5 mg increments, and providing respiratory supportive care and inotropic therapy as needed.

B. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) causes water retention with continued urinary excretion of Na. This leads to dilutional hyponatremia, decreased serum osmolality, increased urine osmolality, and decreased urinary output. Water retention and serum hypo-osmolality might progress to water intoxication, which leads to non-specific signs such as nausea, vomiting, headache, irritability, disorientation, seizures, and coma.

Treatment consists of water restriction, loop diuretics, and hypertonic saline. In mild cases, fluid restriction (1 to 1.5 L/day) is sufficient to correct hyponatremia. Furosemide may be added because it impairs the kidney’s ability to concentrate urine. Hypertonic saline is usually reserved for a serum Na < 120 to 125 mEq/L. It is given in small amounts for a short time (1 to 2 mL/kg/hour for 2 to 3 hours) after which serum Na and osmolality are measured. During the acute phase of SIADH, urine output is measured hourly and urine osmolality and specific gravity and serum Na and osmolality are measured every 6 to 8 hours. Serum Na should be increased at a rate of no more than 0.5 mEq/L/hour or 12 mEq/L/day. Faster rates of correction may cause osmotic demyelination, which develops over several days. Osmotic demyelination is associated with non-specific signs such as behavioral changes, movement disorders, seizures, pseudobulbar palsy, quadriparesis, and coma.

C. Spinal cord injury (SCI) occurring in conjunction with head injury might become apparent only in the postoperative period. Up to 15% of head-injured patients sustain cervical spine injury as well. Precautions to avoid exacerbation of SCI are continued in the postoperative period until cervical spine injury has been ruled out or repaired. Pharmacologic therapy to ameliorate SCI may be given within 8 hours of injury in the form of methylprednisolone, loading dose 30 mg/kg intravenously; then 5.4 mg/kg/hour intravenously for 23 hours. Acute phase spinal shock, which is usually present during the first week from injury, is treated with fluids, inotropes, and pressors. During the chronic phase of spinal injury after the first week, adequate analgesia is provided before somatic or splanchnic stimulation in patients who have injury above T6 to avoid the risk of autonomic hyper-reflexia.

D. Cardiovascular and respiratory monitoring, in conjunction with the appropriate imaging and laboratory studies, is aimed at detecting extracranial injuries and complications such as pneumothorax, hemothorax, intra-abdominal or retroperitoneal hemorrhage, and fat embolism.

E. Prevention of secondary brain injury is continued in the postoperative period. Hypotension, hypoxia, hyperthermia, hyperglycemia, hypoglycemia, increased ICP, and any aggravating factors such as pain, nausea, vomiting, seizures, hypertension, hypercarbia, and impaired cerebral venous drainage should all be prevented and treated. Conscious, mechanically ventilated patients are sedated with short-acting drugs, such as propofol, 10 to 30 mcg/kg/ minute intravenously, or dexmedetomidine, loading dose 1 mcg/kg intravenously over 10 minute; then 0.2 to 0.7 mcg/kg/hour for < 24 hours, to allow intermittent neurologic assessment. Pain from the operative procedure or the primary or associated injury is relieved with opioids such as morphine, 0.05 mg/kg, or fentanyl, 0.5 to 1 mcg/kg. Nausea and vomiting are treated with stomach suctioning through the mouth because of the potential for skull base fracture. Pharmacologic therapy includes ondansetron, 4 mg intravenously, dolasetron, 12.5 to 25 mg, or granisetron, 0.1 to 1 mg. Seizure prophylaxis after head trauma is somewhat controversial. Phenytoin, loading dose 15 mg/kg intravenously over 20 minute followed by 5 to 7 mg/ kg/day, or fosphenytoin, loading dose “phenytoin equivalent (PE)” 15 to 20 mg/kg intravenously; then 4 to 6 PE mg/kg/day, may be given for 2 weeks after head injury if there have been no seizures or longer if there have.

F. Clotting may be impaired because of the release of tissue thromboplastin and a trauma-induced decrease in platelets, prothrombin (factor II), proaccelerin (factor V), and plasminogen, and an increase in fibrin degradation products (FDPs).

V. COMPLICATIONS AFTER OPERATION FOR ANEURYSM

A. Vasospasm. Angiographic narrowing of blood vessels occurs in about 30% of patients between days 4 and 14 after subarachnoid hemorrhage (SAH). Neurologic dysfunction (disorientation, decreased level of consciousness, focal deficit) occurs in about 50% of patients who have angiographic narrowing. The risk for developing vasospasm correlates with the amount of blood around the circle of Willis, the preoperative use of antifibrinolytic therapy, and the postoperative development of the cerebral salt wasting (CSW) syndrome. Pharmacologic prophylactic therapy for vasospasm is initiated within 96 hour of SAH and consists of nimodipine, 60 mg by mouth every 4 hour for 21 days or longer. A CT angiogram or traditional angiography should be performed to confirm the diagnosis of vasospasm. A CT scan can also rule out other potential etiologies of altered consciousness such as recurrent hemorrhage and hydrocephalus. “Triple-H” therapy (hypervolemia, hypertension, and hemodilution) for the treatment of vasospasm after SAH consists of the administration of crystalloid and colloid solutions to achieve a pulmonary capillary wedge pressure of 12 to 16 mm Hg and a hemoglobin of 11 g/dL and the use of inotropes and vasopressors to achieve a mean arterial pressure (MAP) of 120 mm Hg or more. Antidiuretic therapy with vasopressin is sometimes necessary to prevent the diuresis induced by volume loading. Hypotension, heart failure, myocardial ischemia, and pulmonary edema are occasional complications of Triple-H therapy.

B. Obstructive hydrocephalus from subarachnoid blood-induced disturbances in CSF circulation may occur after SAH. The resulting increase in ICP may be manifest as a decreased level of consciousness. A CT scan is diagnostic and ventriculostomy with CSF drainage is the effective therapy. Increased ICP, particularly if the ICP does not respond to treatment, is associated with a less favorable outcome.

C. Hyponatremia after SAH can be due to the cerebral salt-wasting (CSW) syndrome or, less commonly, to SIADH. The CSW syndrome is caused by increased secretion of atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide. These peptides suppress aldosterone synthesis and lead to natriuresis, diuresis, and vasodilatation. Hyponatremia in the CSW syndrome results from increased renal excretion of Na (150 to 200 mEq/L), which is followed by water with resultant hypovolemia. The hyponatremia of SIADH is mainly a result of water retention in conjunction with the renal excretion of Na in a range of 20 to 30 mEq/L.

Treatment of the two forms of hyponatremia is completely different. Patients who have CSW require Na replacement and fluid administration, whereas patients who have SIADH require fluid restriction and diuresis. Fluid restriction and diuresis in a patient who has CSW can be fatal due to the possibility of severe hypovolemia and cerebral infarction. Fluid and salt administered to a patient who has SIADH may lead to osmotic demyelination. Hypertonic saline may be used with close monitoring of serum Na in both cases.

D. Diabetes insipidus occurs less frequently than CSW syndrome or SIADH after SAH (see Section III.A). Treatment includes hypotonic fluids in the form of enteral free water or parenteral D₅W, D₅ 0.2% NaCl, or 0.45% NaCl plus the administration of 1-deamino-8-d-arginine vasopressin, 0.3 mcg/kg/day intravenously or subcutaneously in two divided doses; 0.05 to 1.2 mg/day by mouth; or 10 to 40 mcg/day or three times a day as a nasal spray.

E. Intracranial hematomas might develop at the operative site or at the dural bridging veins from overzealous CSF drainage. Manifestations are those of increased ICP, which may be associated with focal deficit. CT scan is diagnostic and treatment with surgical evacuation may be required.

F. Seizure prophylaxis is continued in the postoperative period owing to the high risk of seizures after SAH, especially in hypertensive patients. Phenytoin is usually given for 3 to 6 months after SAH. Levetiracetam may be used in patients who have serious adverse reactions to phenytoin.

G. Neurogenic pulmonary edema occurs in some patients after SAH because of the sudden increase in ICP, which produces intense sympathetic activation, catecholamine release from the hypothalamus and the medulla, and increased pulmonary vascular pressure and permeability (see Section IV.A). Diagnosis

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