Complications
Often associated with over-confidence or risk-taking while under the influence of psychostimulant drugs. Signs of traumatic injury are important to see in amfetamine overdose, as they may complicate the clinical picture and management.[60]
Acute kidney injury in the clinical setting of hyperthermia is thought to be multifactorial. Muscle injury releases myoglobin, uric acid, and myocyte cytosol contents into the plasma. Pigmented casts form in renal tubules, which results in obstruction, and direct toxicity to tubules occurs through the haem components of myoglobin. Renal ischaemia results from the vasoconstriction of renal arterioles in an underperfused state. Hydration is paramount to management, and diuretics may be helpful in maintaining urine output. Severe cases may require temporary haemodialysis for management. Full recovery is the norm.
Hyperthermia may lead to a clinical picture similar to that of severe heat stroke, with rhabdomyolysis, metabolic acidosis, renal failure, disseminated intravascular coagulation, or acute respiratory distress syndrome.[6][7][8] Management of DIC consists of hydration, control of hyperthermia, and blood product support only if active bleeding is taking place (balance risk of precipitating clotting cascade versus benefit of use of products). Consultation with a haematologist is best sought when disseminated intravascular coagulation is diagnosed.[56]
Acute dyspnoea and hypoxaemia, which progress to respiratory failure, and bilateral infiltrates on chest x-ray, may follow hyperthermia. Hypoxaemia with PaO₂ to inspired oxygen ratio ≤200 and no clinical evidence of heart failure are characteristic. Low tidal volume with plateau pressure-limited mechanical ventilation is the only therapy that has been shown to reduce mortality.
Sympathetic over-stimulation and hypertension are implicated in cerebral and intracranial bleeding of amfetamine toxicity. CT and MRI scans, with high sensitivity for intracerebral haemorrhage, are definitive in differential diagnosis.
Nausea and malaise are the earliest findings, and may be seen when the plasma sodium concentration falls below 125-130 mmol/L (125-130 mEq/L).[88] This may be followed by headache, lethargy, and obtundation. If untreated, seizures, coma, and respiratory arrest may ensue. Treatment with fluid restriction is adequate in most cases, with hypertonic saline an option if urgent intervention is necessary. Vasopressin receptor antagonists are an alternative to fluid restriction and hypertonic saline solution.
Severe neurological symptoms, such as altered mental status, seizure, and coma, may result. These are treated with hypertonic saline, with close monitoring to avoid over-correction of serum sodium.
Very rarely reported, thought to be due to ingestion of MDMA (ecstasy). It is usually self-limiting and managed expectantly.[90]
Can occur after chronic exposure to amfetamines. It is characterised by breathlessness and fatigue, and may be diagnosed by transthoracic echocardiography. Treatment with diuretics and afterload reduction is the norm. Drug cessation may resolve early cardiomyopathy; otherwise, this complication is permanent and a cause of significant morbidity in users of amfetamines.[26][52][53][54][55][89]
Use of this content is subject to our disclaimer