Poisoning with the organophosphate malathion can cause serious complications and possibly even death. This toxic substance is a common insecticide and an ingredient in certain treatment products for head lice.
The timing and onset of symptoms in individuals with organophosphate poisoning depend on the dose, duration, and route of exposure of the specific toxic substance . Children typically present with seizure and coma while adults are more likely to manifest with muscarinic or nicotinic effects . The acute clinical picture traditionally features salivation, lacrimation, urination, defecation, gastric cramps, and emesis (SLUDGE).
Among the wide spectrum of CNS symptoms, patients may experience seizures, various types of paralysis, cranial nerve palsies, and muscle weakness  as well as muscle twitching and cramping. Neuropsychiatric symptoms include fatigue, anxiety, irritability, confusion, lethargy, cognitive impairment, loss of consciousness, and possibly coma .
Patients are very likely to develop respiratory manifestations such as wheezing, increased bronchial secretions, bronchospasm, bronchial narrowing, and respiratory depression . They are also at risk for cardiovascular effects such as bradycardia, tachycardia, hypertension, hypotension, and arrhythmia .
The leading causes of death are respiratory paralysis and cardiac arrest  .
The vital signs will be notable for abnormal heart rate and/or rhythm as well as blood pressure extremes. Additionally, mental status changes will be apparent. Patients may exhibit pinpoint pupils, slurred speech, gait ataxia, and a broad range of neurologic, respiratory, and behavioral symptoms.
When evaluating a patient with clinical features suspicious for organophosphate poisoning, the medical team should assess and manage the patient urgently. The clinicians must inquire about the exposure route and the amount of malathion while also obtaining the history and conducting the physical exam. The diagnosis is mainly clinical but malathion poisoning is confirmed through the appropriate studies.
The definitive diagnostic tool is the measurement of cholinesterase activity. There are two types of assays, butyrylcholinesterase (also referred to as plasma cholinesterase and pseudocholinesterase) and red blood cell (RBC) acetylcholinesterase . The activity of the former does not correlate to the clinical severity . However, RBC acetylcholinesterase is likely a good indicator of the severity .
A comprehensive workup will also include a complete blood count (CBC) and complete metabolic panel (CMP), which would reveal leukocytosis, hypokalemia, hypomagnesemia, hyperglycemia , increased liver function tests (LFTs), and elevated amylase . Furthermore, an arterial blood gas (ABG) is crucial; this will demonstrate respiratory and/or metabolic acidosis. Additionally, myocardial enzymes will show elevated troponin .
The clinical manifestations will reflect which imaging modalities should be performed. For example, respiratory symptoms are investigated with a chest x-ray, which displays pulmonary edema in affected patients.
Since cardiac involvement is common, an electrocardiogram (EKG) is an essential study. Abnormalities may include ST segment changes , inverted T waves, torsade de points and ventricular fibrillation . Sinus tachycardia is a frequent finding initially, but this transforms to sinus bradycardia as the toxicity progresses.