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.
Signs of shock in children and young people include:[9][50][52]
Capillary refill time >2 seconds
Abnormal skin colour
Tachycardia and/or hypotension
Respiratory symptoms or breathing difficulty
Cold hands/feet
Toxic/moribund state
Altered mental status/decreased consciousness
Decreased urine output (<1 mL/kg/h)
Hypoxia on arterial blood gas
Base deficit (worse than -5 mmol/L)
Increased lactate (>2 mmol/L).
Resuscitation should follow the principles of paediatric and adult advanced life support, with evaluation of the patient's airway, breathing, and circulatory status, and establishment of secure large-calibre intravenous catheters for administration of fluids and antibiotics.[74][77] Inotropic medicines should be administered to patients with hypotension or poor perfusion who do not respond promptly to fluid resuscitation.[77]
The possibility of adrenal haemorrhage should be considered.
Local inflammatory responses to bacteria, altered cerebral blood flow, and vasculitis lead to cerebral oedema.[91] Lumbar puncture is contraindicated in patients suspected of having elevated ICP.
Signs of raised intracranial pressure include:[51][52]
Reduced or fluctuating level of consciousness (Glasgow Coma Scale score <9 or drop of ≥3)
In children unable to give a verbal response (in practice, those under 2 years), use the Glasgow Coma Scale with modification for children.[9] Glasgow Coma Scale: modification for children Opens in new window
Relative bradycardia and hypertension
Focal neurological signs
Abnormal posture or posturing
Seizures
Unequal, dilated, or poorly responsive pupils
Papilloedema (late sign)
An enlarged blind spot may be identified when you examine the visual fields
Abnormal ‘doll’s eye’ movements
Follow local or national protocols to treat raised intracranial pressure in children and young people.[9] Adult 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.
Occur in 9% to 34% of neonates and 10% to 56% of children with bacterial meningitis.[52][53] Reported in 5% to 20% of patients with meningococcal meningitis.[46] One or more neurological complications (impairment of consciousness, seizures, or focal neurological abnormalities) are seen in up to 40% of patients with meningococcal meningitis at some point in the clinical course.[55]
Follow local or national protocols to treat seizures in children and young people with suspected bacterial meningitis.[9] In adults 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 haemorrhagic complications of infection.
Moderate to severe hearing loss occurs in up to 10% of childhood survivors of meningococcal meningitis.[92]
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.
Ensure children and young people are reviewed by a paediatrician (with the results of their hearing test) 4-6 weeks after hospital discharge to discuss morbidities associated with their condition and be offered referral to appropriate services.[9]Children with hearing loss are at risk of further developing balance disturbances and speech and language delay, which can lead to long-term behavioural problems.[93][94]
Vasculitis, intravascular thrombosis, cerebral oedema, and direct toxicity to neurons may cause these neurological sequelae.
Subtle consequences that may not be apparent for several years after infection. Around 20% to 30% of children who have had bacterial meningitis go on to develop academic and behavioural problems and 10% to 20% have significant cognitive impairment overall.[87][88][89][90] However, neurological complications are more common in lower- and middle-income countries due to delayed presentation to medical services, lack of access to health care, and limited resources.[90]
Early detection and referral for rehabilitation is important to ensure optimal outcomes. Survivors of severe meningococcal infections may have emotional, learning, and behavioural disorders that require multi-disciplinary assessment and treatment. Affected children may require multi-disciplinary assessment and treatment.
Vasculitis, intravascular thrombosis, and tissue oedema may lead to ischaemic necrosis of skin, compartment syndrome, or other ischaemic injury to extremities. These injuries may require surgical debridement or skin grafting and should be managed in collaboration with experienced plastic and orthopaedic surgeons.
Acute adrenal insufficiency may be caused by adrenal haemorrhage, 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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