Complications
Hypotension results from increased vascular permeability and, in the later stages of the illness, dysregulation of vascular tone. Both myocarditis and myocardial depression may contribute to poor tissue perfusion. Resuscitation should follow the principles of pediatric and adult advanced life support, with evaluation of the patient's airway, breathing, and circulatory status, and establishment of secure large-caliber intravenous catheters for administration of fluids and antibiotics.[51][74] Inotropic medications should be administered to patients with hypotension or poor perfusion who do not respond promptly to fluid resuscitation.[74]
The possibility of adrenal hemorrhage should be considered.
Local inflammatory responses to bacteria, altered cerebral blood flow, and vasculitis lead to cerebral edema. Lumbar puncture is contraindicated in patients suspected of having elevated ICP.
Patients with evidence of elevated ICP should be intubated and ventilated to maintain adequate oxygenation and normocapnia. Patients should be positioned with heads elevated 30° and in a midline position, and stimuli reduced by sedation and minimal handling.
Seizures should be treated aggressively.
Mannitol, furosemide, dexamethasone, and short periods of hyperventilation may be indicated for the acute treatment of severely elevated ICP.
Seizures should be treated aggressively with benzodiazepines. Patients with seizure disorders generally require long-term anticonvulsant therapy.
Disseminated intravascular coagulation (DIC) is caused by acquired deficiencies of protein C, protein S, and antithrombin III; increases in plasminogen activator inhibitor and thrombin-activatable fibrinolysis inhibitor; and reduced activation of protein C on endothelial cells.
Coagulation defects are corrected by fresh frozen plasma, coagulation factor concentrates, and platelet or cryoprecipitate infusion, to reduce the likelihood of hemorrhagic complications of infection.
Moderate to severe hearing loss occurs in 2% to 10% of survivors of meningococcal meningitis.
Local inflammatory responses damage cochlear nerves, resulting in sensorineural hearing loss. The severity may vary from mild to profound, and hearing loss may be unilateral or bilateral.
Vasculitis, intravascular thrombosis, cerebral edema, and direct toxicity to neurons may cause these neurologic sequelae. Early detection and referral for rehabilitation is important to ensure optimal outcomes. Survivors of severe meningococcal infections may have emotional, learning, and behavioral disorders that require multidisciplinary assessment and treatment.
Vasculitis, intravascular thrombosis, and tissue edema may lead to ischemic necrosis of skin, compartment syndrome, or other ischemic injury to extremities. These injuries may require surgical debridement or skin grafting and should be managed in collaboration with experienced plastic and orthopedic surgeons.
Acute adrenal insufficiency may be caused by adrenal hemorrhage, and functional adrenal insufficiency may occur in patients with sepsis. Patients with refractory symptoms of shock should receive replacement doses of corticosteroids until adrenal insufficiency can be excluded.
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