After reading this note you will be able to recognise common toxic and drug‑reaction presentations in Kenyan hospitals, order the appropriate initial investigations, grade severity and initiate the correct immediate and definitive management while knowing which local guidelines to consult.
Definition
Poisoning – the harmful effect on the body after exposure to a chemical, drug, plant, animal toxin or environmental agent, whether intentional, accidental or occupational.
Adverse drug reaction (ADR) – any noxious, unintended response to a medication at doses normally used for prophylaxis, diagnosis or therapy. ADRs are classified as:
| Type | Description |
|---|---|
| A (dose‑related) | Predictable, related to pharmacologic action |
| B (bizarre) | Unpredictable, immune‑mediated or idiosyncratic |
| C (chronic) | Result of long‑term use |
| D (delayed) | Appear after drug discontinuation |
| E (withdrawal) | Due to abrupt cessation |
| F (failure) | Unexpected lack of therapeutic effect |
Anatomy and physiology you need
| System | Relevance to poisoning/ADRs |
|---|---|
| Gastro‑intestinal mucosa | Absorption site; barrier to toxins; vomiting reflex |
| Liver (hepatocytes, CYP450) | Phase I/II metabolism; bioactivation or detoxification |
| Kidneys (glomeruli, tubules) | Excretion of unchanged drug and metabolites; renal tubular reabsorption of weak acids/bases |
| Cardiovascular system | Distribution via blood; toxin‑induced arrhythmias, hypotension |
| Central nervous system (BBB, brainstem) | Site of many neurotoxic effects; altered consciousness |
| Respiratory system | Ventilation removes volatile agents; pulmonary edema in some poisonings |
| Skin & mucous membranes | First‑line decontamination; signs of exposure (e.g., erythema, burns) |
Causes and risk factors
| Category | Common agents in Kenya | Specific risk factors |
|---|---|---|
| Household chemicals | Organophosphates (pesticides), bleach, kerosene | Rural farming, poor storage |
| Traditional medicines & herbs | Mitragyna speciosa, Artemisia spp., herbal concoctions | Cultural practices, self‑medication |
| Pharmaceuticals (over‑the‑counter) | Paracetamol, NSAIDs, antimalarials, antiretrovirals, anti‑TB drugs | Polypharmacy, HIV/TB co‑treatment, self‑prescribing |
| Occupational exposures | Lead, mercury, solvents | Mining, battery recycling, paint work |
| Food‑borne toxins | Aflatoxin, cyanogenic glycosides (cassava) | Improper storage, famine conditions |
| Intentional overdose | Tricyclic antidepressants, antipsychotics, barbiturates | Psychiatric illness, substance abuse |
| Disease‑related susceptibility | HIV (immune dysregulation), TB (liver disease), malaria (hemolysis), sickle cell disease (renal impairment), rheumatic fever (cardiac involvement) | Co‑morbid organ dysfunction, drug‑drug interactions |
Pathophysiology
Poisoning
Exposure → Absorption (GI, dermal, inhalation) → Distribution (blood → target organs) → Metabolism (activation or detox) → Excretion → Cellular injury (membrane disruption, enzyme inhibition, oxidative stress) → Clinical syndrome
Adverse drug reaction
Drug administration → Pharmacologic interaction with receptors/enzymes → Predictable effect (type A) or immune/idiopathic response (type B) → Cellular dysfunction or hypersensitivity → Symptom manifestation
Clinical features
| History element | Why it matters |
|---|---|
| Time line of exposure – exact time of ingestion, inhalation, dermal contact or iatrogenic administration | Determines window for decontamination, predicts onset of symptoms (early vs delayed) and helps estimate severity |
| Substance identity – name (brand/generic), formulation, concentration, amount (if known) | Guides specific antidote use, predicts organ systems at risk and informs toxicokinetic expectations |
| Route of exposure – oral, IV, IM, inhalation, dermal, rectal | Influences absorption rate, first‑pass metabolism and need for activated charcoal or gastric lavage |
| Co‑ingestants / polypharmacy – other drugs, alcohol, traditional medicines | Synergistic toxicity (e.g., CNS depression with alcohol) and risk of drug‑drug interactions |
| Pre‑existing conditions – HIV, TB, malaria, rheumatic disease, sickle‑cell disease, chronic liver or renal disease | Altered metabolism, reduced clearance and increased susceptibility to organ injury |
| Intent – accidental vs deliberate | Affects need for psychiatric assessment and possible repeat exposure |
| Symptoms at presentation – nausea, vomiting, abdominal pain, altered mental status, seizures, cardiac arrhythmia, respiratory distress, skin changes | Correlates with organ systems involved and helps prioritize investigations |
| Recent treatments – antiretrovirals, anti‑TB drugs, antimalarials, disease‑modifying agents | Some have narrow therapeutic windows and can cause toxicity at therapeutic doses (e.g., isoniazid, quinine) |
Examination findings and pathophysiologic basis
| Finding | Pathophysiologic explanation |
|---|---|
| Altered level of consciousness (drowsiness, agitation, coma) | Direct CNS depressant effect, hypoxia, metabolic encephalopathy, seizures |
| Pupil size/reactivity – pinpoint, dilated, sluggish | Opioids → miosis; anticholinergics, sympathomimetics → mydriasis; brainstem involvement |
| Skin – flushing, diaphoresis, pallor, rash, bullae, necrosis | Vasodilation or vasoconstriction, histamine release, direct cytotoxicity, metabolic acidosis |
| Cardiovascular – tachycardia, bradycardia, hypotension, hypertension, arrhythmias | Catecholamine excess, direct myocardial toxicity, electrolyte disturbances |
| Respiratory – tachypnea, bronchospasm, pulmonary edema, apnea | Central respiratory depression, airway irritation, fluid shifts, aspiration |
| Abdominal – tenderness, guarding, ileus | Gastric irritation, pancreatitis, hepatic congestion |
| Neurological – tremor, fasciculations, seizures, peripheral neuropathy | Neuroexcitatory toxins, cholinergic excess, demyelination from metabolic derangement |
| Renal – oliguria, flank pain | Acute tubular necrosis from nephrotoxic agents, hemoglobinuria/myoglobinuria |
| Hepatic – jaundice, hepatomegaly | Direct hepatocellular injury, cholestasis |
Differential diagnosis
| Condition | Points toward it | Distinguishing feature |
|---|---|---|
| Acute organophosphate poisoning | Salivation, lacrimation, bronchorrhea, muscle fasciculations, history of pesticide exposure | Presence of cholinergic crisis; improves with atropine and oximes |
| Opioid overdose | Pinpoint pupils, respiratory depression, history of opioid use | Reversal with naloxone; rapid improvement |
| Anticholinergic toxicity (e.g., tricyclics, antihistamines) | Hyperthermia, dry skin, dilated pupils, urinary retention, delirium | Absence of sweating; improves with physostigmine |
| Salicylate poisoning | Tinnitus, hyperventilation, metabolic acidosis, fever, recent aspirin use | Respiratory alkalosis early, then anion‑gap acidosis |
| Carbon monoxide poisoning | Headache, cherry‑red skin, exposure to smoke/poor ventilation | Elevated carboxyhaemoglobin; improves with 100% O₂ |
| Methemoglobinemia | Cyanosis unresponsive to O₂, chocolate‑brown blood, exposure to nitrates or dapsone | Pulse oximetry reads ~85%; responds to methylene blue |
| Acute kidney injury from nephrotoxins (e.g., aminoglycosides, NSAIDs) | Oliguria, flank pain, recent drug use, elevated creatinine | Urine sediment (granular casts) and lack of systemic CNS signs |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Blood gas (ABG) with electrolytes | Acid‑base status, respiratory compensation, electrolyte derangements | Metabolic acidosis with anion gap → salicylates, methanol; respiratory alkalosis → early salicylates |
| Serum drug/toxin level (e.g., acetaminophen, digoxin, lithium) | Confirms exposure, guides antidote threshold | Level above toxic threshold → initiate specific therapy |
| Complete blood count | Hematologic toxicity, infection | Leukocytosis may suggest infection or stress; anemia in hemolysis |
| Liver function tests | Hepatocellular injury | ALT/AST > 3× ULN suggests hepatic toxin (e.g., paracetamol) |
| Renal function (creatinine, urea, electrolytes) | Nephrotoxicity, need for dialysis | Rising creatinine with oliguria → consider renal replacement |
| ECG | Cardiac toxicity, QT prolongation, arrhythmias | Prolonged QT → quinidine, anti‑malarial; ST changes → coronary spasm from cocaine |
| Chest X‑ray | Aspiration, pulmonary edema, pneumothorax | Bilateral infiltrates → pulmonary edema from fluid overload or toxin |
| Urine toxicology screen | Presence of common drugs of abuse, some antimalarials | Positive for cocaine, amphetamines, etc., supporting diagnosis |
Diagnosis and severity
- Establish the toxic exposure – combine history (substance, dose, route, timing) with clinical picture and confirmatory laboratory data.
- Classify severity (adapted from common toxicology grading):
| Severity | Clinical criteria |
|---|---|
| Mild | Minimal symptoms (e.g., mild nausea, transient dizziness), normal vitals, no organ dysfunction, toxin level below established toxic threshold. |
| Moderate | Persistent gastrointestinal symptoms, mild CNS changes (confusion, tremor), mild tachycardia or hypertension, laboratory abnormalities not yet causing organ failure (e.g., mild transaminitis, modest metabolic acidosis). |
| Severe | Life‑threatening manifestations: respiratory depression, seizures, hemodynamic instability, marked metabolic derangement, organ failure (acute liver or renal failure), toxin level well above toxic threshold. |
- Document – record exact substance, estimated amount, time of exposure, clinical grade, investigations performed, and initial management steps. This forms the basis for ongoing monitoring, definitive therapy, and medico‑legal reporting.
Key points for the junior clinician
- Early recognition hinges on a focused history that captures timing, route, and co‑morbidities common in Kenya (HIV, TB, malaria).
- Physical signs often reflect the pharmacologic action of the toxin; linking pupil size, skin colour, and cardiovascular status to the suspected agent narrows the differential.
- Basic investigations (ABG, ECG, LFTs, renal panel) are usually available and give rapid insight into severity.
- Antidotes are toxin‑specific; when unavailable, supportive care (airway protection, seizure control, fluid resuscitation) remains the cornerstone.
- Continuous reassessment is essential because many poisonings have biphasic courses (e.g., early CNS depression followed by delayed hepatic injury).
By systematically integrating history, examination, targeted investigations and severity grading, the medical officer can deliver timely, evidence‑based care and mitigate the high morbidity associated with poisoning and adverse drug reactions in our setting.
Management
Immediate stabilisation
| Step | Action | Rationale |
|---|---|---|
| Airway | Position, suction, or secure with endotracheal tube if compromised | Prevent aspiration of vomitus or caustic material |
| Breathing | Give high‑flow oxygen, assess for bronchospasm or pulmonary edema | Correct hypoxia, treat airway irritation (e.g., bronchodilators for organophosphate bronchospasm) |
| Circulation | Large‑bore IV/IO line, isotonic fluids, treat hypotension | Restore perfusion; many poisons cause vasodilation or myocardial depression |
| Decontamination | Activated charcoal (if within appropriate time and airway protected) or gastric lavage for life‑threatening ingestion | Reduces systemic absorption |
| Antidotes (if indicated) | e.g. atropine for organophosphates, naloxone for opioid overdose, N‑acetylcysteine for paracetamol, fomepizole for toxic alcohols | Counteract specific toxin mechanisms |
| Seizure control | Benzodiazepine (IV/IM) for toxin‑induced seizures | Prevent secondary brain injury |
Definitive treatment
- Identify the toxin – history, container, regional epidemiology (e.g., pesticide exposure in rural Kenya, traditional herbal preparations).
- Targeted antidote – give as early as possible; repeat dosing according to clinical response.
- Enhance elimination – forced diuresis, haemodialysis, or charcoal hemoperfusion for toxins cleared renally or dialyzable (e.g., methanol, lithium).
- Support organ function – inotropic support for cardiogenic shock, mechanical ventilation for respiratory failure, renal replacement for acute kidney injury.
Monitoring & safety
- Continuous ECG, pulse oximetry, capnography if intubated.
- Serial vitals, urine output, mental status checks every 15‑30 min initially.
- Laboratory trend: electrolytes, renal and liver panels, lactate, arterial blood gases.
- Observe for antidote toxicity (e.g., atropine‑induced tachycardia, naloxone‑precipitated withdrawal).
- Ensure safe disposal of contaminated materials; wear gloves and eye protection when handling caustics or chemicals.
Contra‑indications & safety notes
- Activated charcoal is contraindicated in compromised airway, ingestion of caustics, or hydrocarbon liquids.
- Gastric lavage only if life‑threatening ingestion and within 1 hour; avoid in perforated viscus suspicion.
- Antidotes should not be given if the suspected toxin is not confirmed and the drug carries significant adverse effects (e.g., fomepizole in non‑alcoholic poisoning).
Complications and prognosis
- Acute organ failure – hepatic necrosis (paracetamol), acute tubular necrosis (heavy metals), ARDS (inhalational toxins).
- Neurological sequelae – peripheral neuropathy (organophosphates), delayed encephalopathy (carbon monoxide).
- Cardiovascular collapse – arrhythmias, myocardial depression (cocaine, tricyclic antidepressants).
- Metabolic derangements – severe acidosis (methanol, ethylene glycol), electrolyte shifts (salicylates).
- Long‑term sequelae – chronic kidney disease after heavy‑metal exposure, psychiatric sequelae after intentional overdose.
Prognosis hinges on time to presentation, availability of antidote, and extent of organ damage. Early decontamination and antidote administration markedly improve outcomes; delayed care often leads to irreversible injury or death.
High‑yield exam points
- Look‑alike conditions:
- Commonest wrong first step: administering activated charcoal without securing the airway in a patient with decreased consciousness.
- Examiner bedside questions:
- “What is your immediate airway plan for a patient with a caustic ingestion and a GCS of 8?”
- “Explain why you would give atropine before pralidoxime in organophosphate poisoning.”
- “How does the regional prevalence of pesticide poisoning influence your differential?”
Clinical case
Case: A 28‑year‑old male farmer presents 45 minutes after accidental ingestion of an unknown pesticide. He is drowsy, drooling, with pinpoint pupils, diffuse sweating, and fasciculations. Blood pressure 100/60 mmHg, heart rate 110 bpm, respiratory rate 22 /min, SpO₂ 96% on room air.
Questions
- What is the first pharmacologic intervention and why?
Answer: Atropine – it antagonises muscarinic effects (bronchorrhoea, bronchospasm, bradycardia) and should be given promptly, titrated to drying of secretions and resolution of bronchospasm.
- Which antidote should be added and what is the timing of its administration?
Answer: Pralidoxime – reactivates acetylcholinesterase if given before “aging” of the organophosphate; start as soon as possible after atropine, usually within the first hour.
- What monitoring parameters are essential in the first 6 hours?
Answer: Airway patency, respiratory rate and oxygenation, heart rate and rhythm, blood pressure, pupil size, mental status, and serial cholinesterase levels if available.
Practice questions
Question 1
A 4‑year‑old girl is brought after ingesting an unknown amount of a household cleaning agent (alkaline). She is vomiting, has oral burns, and a GCS of 13. What is the most appropriate next step?
A. Give activated charcoal
B. Perform gastric lavage
C. Endotracheal intubation with cuffed tube
D. Start intravenous proton‑pump inhibitor
Answer: C. Endotracheal intubation with cuffed tube – airway protection is priority because caustic ingestion can cause rapid airway edema; charcoal and lavage are contraindicated.
Question 2
A 55‑year‑old man on chronic isoniazid therapy for TB presents with seizures and a serum lactate of 6 mmol/L. Which treatment should be given immediately?
A. Sodium bicarbonate infusion
B. Pyridoxine (vitamin B6)
C. Intravenous diazepam only
D. Hemodialysis
Answer: B. Pyridoxine (vitamin B6) – it replenishes the co‑factor for GABA synthesis, reversing isoniazid‑induced seizures.
Question 3
A patient with suspected opioid overdose is given naloxone and immediately becomes agitated and hypertensive. What is the most likely explanation?
A. Naloxone toxicity
B. Pre‑existing panic disorder
C. Acute opioid withdrawal
D. Incorrect drug administered
Answer: C. Acute opioid withdrawal – rapid reversal precipitates sympathetic over‑activity, manifesting as agitation and hypertension.
Question 4
Which of the following is a contraindication to the use of activated charcoal in poisoning?
A. Ingestion of a solid tablet >30 minutes ago
B. Patient is alert and oriented
C. Ingestion of a hydrocarbon (e.g., gasoline)
D. Presence of a single‑dose acetaminophen overdose
Answer: C. Ingestion of a hydrocarbon – risk of aspiration and limited adsorption; charcoal is ineffective for hydrocarbons.
Question 5
A 70‑kg woman presents 2 hours after a massive acetaminophen overdose. Which intervention is indicated despite the elapsed time?
A. Intravenous N‑acetylcysteine infusion
B. Immediate haemodialysis
C. High‑dose vitamin C
D. Oral activated charcoal
Answer: A. Intravenous N‑acetylcysteine infusion – it replenishes glutathione and prevents hepatic injury even when given beyond the classic 8‑hour window.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.