Category Archives: General Management of Poisoning

Basic Principles

The management of a poisoned patient should follow a structured systematic approach focusing on the following major areas[2]: (1) resuscitation and stabilization; (2) history and physical examination, including evaluation for a specific toxidrome; (3) appropriate decontamination of the gastrointestinal tract, skin, and eyes;  (4) judicious use of laboratory tests, electrocardiograms, radiographic studies, and other tests as necessary; (5) administration of specific antidotes, if indicated;  (6) utilization of enhanced elimination techniques for selected toxins; (7) appropriate supportive therapy, specialist consultations, and disposition; (8) good nursing care;  (9) psycho-social assessments; and (10) appropriate follow up where indicated.

Even though they may not appear to be acutely ill, all poisoned patients should be treated as if they have a potentially life-threatening intoxication. However, the priorities of the approach and treatment guidelines should be based with the specific toxidrome and the presenting symptoms in mind. Guidelines applicable for one toxin may be contraindicated in another. Therefore, the treating physician should be aware of the common pitfalls of each step in with respect to the toxin involved.


Resuscitation & Stabilization

The first priorities in the management of seriously poisoned patients are the same as with all patients. The patency of the airway must be ensured, followed by assistance of breathing and support of circulation. Cardiac monitoring, pulse oximetry, and intravenous access should be established as indicated by the patient’s clinical condition. CNS toxicity should also be addresses under stabilization especially in the setting of seizures.


Airway & Breathing

The most common factor contributing to death from drug overdose or poisoning is loss of airway-protective reflexes with subsequent airway obstruction caused by the flaccid tongue, pulmonary aspiration of gastric contents or respiratory arrest. All poisoning patients should be suspected of having a potentially compromised airway irrespective of their presentation[3]. Look for signs of airway obstruction such as dyspnea, air hunger or hoarseness and signs of airway comprise such as stridor, intercostal/ subcostal retractions, cyanosis, diaphoresis, and tachypnea.

Along with airway problems, breathing difficulties are the major cause of morbidity and death in patients with poisoning or drug overdose. Patients may have one or more of the following complications[3]:

a) Ventilatory failure from toxins that cause failure of the ventilatory muscles (Eg. organophosphates), central depression of respiratory drive (Eg. opiates), and severe pneumonia or pulmonary edema (Eg. hydrocarbons).

b) Hypoxia (Eg. Cyanide, methemoglobinemia, carbon monoxide).

c) Bronchospasm (Eg. organophosphates).

Airway management should focus on correcting hypoxia and respiratory acidosis and avoiding pulmonary aspiration[2]. Continuous arterial blood gas (ABG) analysis should be done. Acidemia due to respiratory depression can exacerbate the toxicity of drugs, such as cyclic antidepressants and salicylates. Certain toxic conditions can pose problems in the performance of standard airway management techniques. For example, severe upper airway injury that occurs following a caustic ingestion may preclude routine endotracheal intubation, necessitating surgical management of the airway. The use of succinylcholine for rapid-sequence intubation can result in prolonged paralysis in patients with organophosphate toxicity. Sometimes, elective intubation may be warranted despite the patient exhibiting no signs of compromise in case of substances that may produce sudden hemodynamic compromise or stridor without prodromal signs, eg, Endosulphan or Super-Vasmol poisoning. Routine ventilator settings may be grossly inadequate for the patient with severe metabolic acidosis who requires significant respiratory compensation.



A. General Assessment and Initial Treatment[3]:

a. Check blood pressure, pulse rate and rhythm: Perform cardiopulmonary resuscitation (CPR) if there is no pulse and perform advanced cardiac life support (ACLS) for arrhythmias and shock. Standard advanced cardiac life support (ACLS) protocols may be inadequate or inappropriate for resuscitation of poisoned patients with life-threatening cardiac dysrhythmias or cardiac arrest. Eg. The use of procainamide is contraindicated for ventricular dysrhythmias caused by cyclic antidepressants and other myocardial sodium channel-blocking agents.

b. Begin continuous electrocardiographic (ECG) monitoring. Arrhythmias may complicate a variety of poisoning (Eg. Oleander), and all patients with potentially cardiotoxic drug poisoning should be monitored in the emergency department or an intensive care unit for at least 6 hours after the ingestion.

c. Secure venous access. Antecubital or forearm veins are usually easy to cannulate and should be done so with large-bore IV cannulas. Alternative sites include femoral, subclavian, internal jugular, and other central veins. Access to central veins allows measurement of central venous pressure and placement of a pacemaker or pulmonary artery lines.

d. Advanced hemodynamic monitoring with CVP, pulmonary capillary wedge pressure (PCWP), and intra-arterial pressure measurement (IAPM).

e. Draw blood for routine studies (see Diagnostic Testing).

f. Begin intravenous infusions as needed and to keep vein open.

g. In seriously ill patients (eg, those who are hypotensive, obtunded, convulsing, or comatose), place a Foley catheter in the bladder, obtain urine for routine and toxicologic testing, and measure hourly urine output.

B. Fluid Resuscitation & Vasopressors: Most hypotensive patients following toxic ingestions respond well to fluid resuscitation. Initial fluid of choice is normal saline and dextrose-normal saline. Sometimes, low-dose vasopressors may be needed (dopamine 5–15 mcg/kg/min). Note that dopamine may be ineffective in some patients with depleted neuronal stores of catecholamines (eg, tricyclic antidepressant overdose) or in cases where alpha-adrenergic receptors may be blocked (phenothiazines). In such cases norepinephrine, 0.1 mcg/kg/min IV may be more effective[3]. Sympathomimetics may also cause refractory arrhythmia in certain toxin-induced myocardial suppression like endosulphan.

C. Dysrhythmias: Common dysrhythmias encountered are bradycardia and atrioventricular (AV) block, QRS interval prolongation, sinus tachycardia, ventricular arrhythmias, torsade de pointes, and ventricular fibrillation. Rule out electrolyte abnormalities and correct any if present.

Do not treat bradycardia or AV block unless the patient is symptomatic[3] (eg, exhibits signs of syncope or hypotension). Administer atropine,  0.01–0.03 mg/kg IV. If this is not successful, use isoproterenol 1–10 mcg/min IV, titrated to the desired rate, or use an emergency transcutaneous or transvenous pacemaker.

For management of ventricular tachycardias, agents that prolong QT interval like Class Ia, Class Ic, and Class III antiarrhythmic drugs are contraindicated as these may predispose to torsades de pointes[3] (although amiodarone is an exception in Class II drugs). Use lidocaine, 1–3 mg/kg IV or amiodarone 300 mg IV or 5 mg/kg in children. For torsades de pointes, administer intravenous magnesium sulfate, 1–2 g in adults, over 20–30 minutes.

D. Hypertension is frequently overlooked in drug-intoxicated patients and often goes untreated[3]. Eg. Anticholinergics (datura, amphetamines). Nicotinic cholinergic stimulators (organophosphates) may initially cause hypertension and tachycardia followed by hypotension and bradycardia. For hypertension with little or no tachycardia, use nitroprusside, 2–10 mcg/kg/min IV. For hypertension with tachycardia, use labetalol (0.2–0.5 mg/kg IV) or esmolol (500 mcg/kg over one minute loading dose followed by 40-200 mcg/kg/min infusion).


CNS Toxicity

A. Seizures[3] Seizures are a major cause of morbidity and mortality from drug overdose or poisoning. Seizures may be single and brief or multiple and refractory. They can cause airway compromise, resulting in apnea or pulmonary aspiration. Multiple or prolonged seizures may cause severe metabolic acidosis, hyperthermia, rhabdomyolysis, and brain damage.

Since most toxins are GABA antagonists, the treatment of choice for toxin-induced seizures are GABA agonists like benzodiazepines[1] (lorazepam, 0.05–0.1 mg/kg IV or midazolam, 0.05–0.1 mg/kg IV. Refractory seizures may be treated with phenobarbitone, 10–15 mg/kg IV; slow infusion over 15–20 minutes (caution as barbiturates may mimic brain death), propofol, 2–5 mg/kg IV followed by 2-4 mg/kg/hour (watch for propofol infusion syndrome) or thiopentone (3-5 mg/kg loading followed by 3-5 mg/kg/hr infusion).

Phenytoin is considered the anticonvulsant of last choice for most toxin-induced seizures[3].

Monitor for cerebral edema, hyperthermia, and rhabdomyolysis. Neuromuscular paralysis with a nondepolarizing neuromuscular blocker may be used to prevent hyperthermia and rhabdomyolysis associated with refractory seizures. Monitor ECG, electrolytes, and blood glucose levels when administering anticonvulsants.

B. Coma and stupor: A variety of drug overdose and poisonings produce coma and stupor. Coma is most often a result of global depression of the brain’s reticular activating system, caused by anticholinergic agents, sympatholytic drugs, generalized CNS depressants, or toxins that result in cellular hypoxia[3]. Hypoglycemia is one of the major causes of coma and bedside glucose testing should be done at the earliest. Coma sometimes represents a postictal phenomenon after a drug- or toxin-induced seizure.

Coma cocktail may be useful in unknown overdoses and where bedside glucose testing is unreliable; dextrose (50% 50 ml IV), thiamine (100 mg in IV bottle or IM), and naloxone (0.1 mg IV, followed by 0.4 mg and 2 mg IV if no response in 2 minutes).

Consider flumazenil only if benzodiazepines are the only suspected cause of coma and there are no contraindications[3]. Be aware that use of flumazenil can precipitate seizures. Do not use analeptics in coma as they may cause seizure and have been proved to be not beneficial.

C. Hypothermia: Hypothermia may mimic or complicate drug overdose and poisonings and should be suspected in every comatose patient. Re-warming should be done slowly (using blankets, warm intravenous fluids, and warmed-mist inhalation) to prevent rewarming arrhythmias[3].

D. Hyperthermia: It may be caused by excessive heat generation because of sustained seizures, rigidity, or other muscular hyperactivity; an increased metabolic rate or impaired dissipation of heat secondary to impaired sweating (eg, anticholinergic agents). Untreated, severe hyperthermia is likely to result in hypotension, rhabdomyolysis, coagulopathy, cardiac and renal failure, brain injury, and death. Survivors often have permanent neurologic sequelae.

Immediate rapid cooling by mechanical means is essential to prevent death or serious brain damage. Begin external cooling with tepid (lukewarm) sponging and fanning. This evaporative method is the most efficient method of cooling. Antipyretics and salicylates are ineffective in controlling toxin-induced hyperthermia and may worsen any hepatic derangements if present and are therefore contraindicated. The most rapidly effective and reliable means of lowering the temperature is neuromuscular paralysis. Administer a nondepolarizing agent such as pancuronium, 0.1 mg/kg IV, or vecuronium,
0.1 mg/kg IV once the patient has been intubated and ventilated[3].

Neuroleptic malignant syndrome (NMS) is a hyperthermic disorder characterized by hyperthermia, muscle rigidity, metabolic acidosis, and confusion. It is seen rarely in organophosphates poisoning and in antipsychotic overdoses. Bromocriptine or dantrolene (1–10 mg/kg IV) are the treatments of choice[3].

E. Agitation, Delirium, or Psychosis: Administer benzodiazepines, midazolam or lorazepam as stat doses.


Anaphylactic and Anaphylactoid Reactions

Examples of toxins that cause anaphylactic or anaphylactoid reactions include pyrethrins, colchicine, additives in chemical formulations etc. These reactions are characterized by bronchospasm and increased vascular permeability that may lead to laryngeal edema, skin rash, and hypotension. Maintain airway and administer epinephrine 0.3–0.5 mg intramuscularly (IM) (children: 0.01 mg/kg, maximum 0.5 mg) for mild-to-moderate reactions and for severe reactions, administer 0.05–0.1 mg IV bolus every 5 minutes or give an infusion starting at a rate of 1–4 mcg/min and titrating upward as needed.  Diphenhydramine and IV corticosteroids may also be used as needed[3].

History And Physical Examination


The history provides critical information in the assessment of the patient with suspected overdose. A history of substances potentially available to a patient or a history of chronic medical illnesses in members of the household gives clues to classes of medications available. Accurate identification of ingestants is particularly important in the patient exposed to agents that have delayed onset of toxic effects, such as most botanicals or pesticides like yellow phosphorus. The physical examination gives important clues to both the severity and the cause of poisoning. Vital sign and mental status abnormalities are important signs of the severity of toxicity and may also suggest the class of toxin involved. Examples include the respiratory depression of barbiturate or opioid poisoning and the tachycardia and hypertension of poisoning with sympathomimetic agents. Characteristic “toxidromes” indicate the presence of agents with cholinergic, anticholinergic, sympathomimetic, and opioid effects. Less specific findings, such as nystagmus, myoclonus, asterixis, and tremor, also suggest various toxins[2].



Decontamination includes surface decontamination of skin and eyes, gut decontamination with limited indications for the use of orogastric lavage, nasogastric suction, and whole-bowel irrigation as discussed below, and administration of suitable adsorbents.

Surface Decontamination

Dermal decontamination is best accomplished with copious amounts of water. All contaminated clothing should be removed and flush exposed areas with copious quantities of tepid (lukewarm) water or saline. Wash carefully behind ears, under nails, and in skin folds. Use soap and shampoo for oily substances. However, the use of water on skin contaminated with metallic sodium, metallic potassium, or phosphorus (white, yellow) may result in further skin injury owing to heat generation and explosive injury. Irrigation of phenol burns with low molecular weight polyethylene glycol is effective. Other therapies, such as topical calcium salts for hydrofluoric acid burns, may be indicated following initial water decontamination. Do not use neutralizing agents for decontamination like alkalis for acid burns as the exothermic reactions produced would only further worsen the situation.

Ocular decontamination can be accomplished with water or normal saline irrigation. If available, instill local anesthetic drops in the eye first to facilitate irrigation. Remove the victim’s contact lenses if they are being worn. After irrigation is complete, check the conjunctival and corneal surfaces carefully for evidence of full-thickness injury. Perform a fluorescein examination of the eye by using a fluorescein dye and a Wood’s lamp to reveal corneal injury and get ophthalmology consultations for severe injuries.

Extreme care must be taken so as not to expose the care providers to potentially toxic and contaminating substances when performing decontamination measures and all care givers should wear adequate protective gear. The effluent from the decontaminations should be properly disposed off.

Gastrointestinal Decontamination

There remains some controversy about the roles of emesis, gastric lavage, and cathartics to decontaminate the gastrointestinal tract. There is little support in the medical literature for gut-emptying procedures, and studies have shown that after a delay of 60 minutes or more, very little of the ingested dose is removed by emesis or gastric lavage. Moreover, recent studies suggest that in the typical overdosed patient, simple oral administration of activated charcoal without prior gut emptying is probably just as effective as the traditional sequence of gut emptying followed by charcoal[3]. Use of emetics like syrup of ipecac is used rarely in the prehospital setting, and virtually never in hospitals[2]. The use of cathartics has been associated with significant morbidity and mortality because of severe electrolyte abnormalities and with limited alteration in clinical outcome, their routine use is no longer recommended.


A. Gastric Lavage:  Although there is little clinical evidence to support its use, gastric lavage is indicated for most botanicals which are slowly absorbed, recently ingested liquid substances, and substances that are not effectively adsorbed by activated charcoal. Orogastric lavage is usually performed with a large bore (36–40F) tube. Nasogastric lavage with a smaller tube such as Ryle’s tube is sufficient for liquid ingestions. Lavage is more likely to be effective if initiated within 30–60 minutes of the ingestion, although it may still be useful several hours after ingestion of agents that slow gastric emptying (eg, salicylates or anticholinergic drugs).

However, it does not reliably remove undissolved pills or pill fragments (especially sustained-release or enteric-coated products). In addition, the procedure may delay administration of activated charcoal and may hasten the movement of drugs and poisons into the small intestine, especially if the patient is supine or in the right decubitus position[3]. Gastric lavage is not necessary for small to moderate ingestions of most substances if activated charcoal can be given promptly.

It is contraindicated in obtunded, comatose or convulsing patients. In such cases, endotracheal intubation with a cuffed endotracheal tube should be performed first to protect the airway. Use of gastric lavage after ingestion of a corrosive substance is controversial; some gastroenterologists recommend that lavage be performed as soon as possible after liquid caustic ingestion to remove corrosive material from the stomach and to prepare for endoscopy, but the risk of perforation outweighs the benefits[1]. Use of excessive volumes of lavage fluid or plain tap water can result in hypothermia or electrolyte imbalance in infants and small children[4].


B. Adsorbents: The most commonly used adsorbent is activated charcoal, sometimes referred to as the universal antidote. Activated charcoal is a highly adsorbent powdered material and is the primary method of gastrointestinal decontamination. It should be administered preferably within 1 hour of toxin ingestion whenever possible[3]. It may be administered as single-dose activated charcoal (SDAC) (1g/kg in an aqueous slurry) or as multiple doses of activated charcoal (MDAC) (1 g/kg initially followed by 0.5g/kg every 4-6h) [4]. Multiple doses of activated charcoal are beneficial in all drugs and toxins known to bind with small volumes of distribution (less than 1 L/kg), low renal clearance, little protein binding, entero-hepatic recirculation of toxic metabolites, and where gastric emptying may be delayed. In most cases, activated charcoal given alone without prior gastric emptying is as effective as or even more effective than emesis and lavage procedures in reducing drug absorption.

Activated charcoal is contraindicated in patients at risk of aspiration with unprotected airways, caustic ingestions, and small bowel obstruction. Ileus without distension is not a contraindication for a single dose of charcoal, but further doses should be withheld[4]. Charcoal is ineffective in hydrocarbons and heavy-metal poisonings. Charcoal is also not indicated in toxins that are rapidly absorbed from the gut.

The adverse effects include potential complications like constipation or intestinal impaction and charcoal bezoar formation, especially if multiple doses of charcoal are given. Distension of the stomach with a potential risk of pulmonary aspiration, especially in a drowsy patient. Also causes severe hypokalemia especially with MDAC and therefore serum potassium has to be monitored regularly.



Other Selected Oral-Binding Agents[3]

Drug or Toxin

Binding Agent(s)


Cellulose sodium phosphate

Chlorinated hydrocarbons

Cholestyramine resin (16g/day)


Cholestyramine resin, Activated charcoal

Heavy metals (arsenic, mercury)

Demulcents (egg white, milk)


Sodium polystyrene sulfonate (Kayexalate) (0.3–0.6 g/kg in sorbitol PO)


Fuller’s earth (1-2g/kg), Bentonite (1 to 2 g/kg), or Activated charcoal – all as an aqueous slurry


Sodium polystyrene sulfonate (Kayexalate)


Prussian blue (150-250 mg/kg/day in divided doses)


C. Whole-Bowel Irrigation: Whole-bowel irrigation has become an accepted method for elimination of some drugs and poisons from the gut. The technique makes use of a surgical bowel-cleansing solution containing a nonabsorbable polyethylene glycol in an isotonic electrolyte solution that is formulated to pass through the intestinal tract without being absorbed[3] [4]. This solution is given at high flow rates to force intestinal contents out by sheer volume. The typical dosing is 500 ml-2000 ml/hour via nasogastric tube (Pediatric dose is 35 ml/kghr) given until the rectal effluent is clear. It may be given along with activate charcoal if the toxin is known to bind to AC. Large volume stools usually occur within 1-2 hours after administration. WBI must be stopped after 8–10 L (children: 150–200 mL/kg) if no rectal effluent has appeared.

It is indicated in large ingestions of iron, lithium, or other drugs poorly adsorbed to activated charcoal, large ingestions of sustained-release or enteric-coated tablets, and ingestion of foreign bodies or drug-filled packets or condoms.

Contraindications include ileus and intestinal obstruction, and obtunded, comatose or convulsing patient unless the airway is protected[4].

Diagnostic Testing


I. Toxicology Screening:  The results of routine toxicology screens seldom add useful information about the toxins involved that has not already been gleaned from the history, and assessment of signs and symptoms. Additionally, the results of screens may be inaccurate. Many toxic agents are not detected on routine screening[2] while false-positive results are commonly reported. Unlike broad toxicology screens, serum concentrations of specific drugs are useful in guiding management, but these are not readily available at most centers, and only delays management. As comprehensive blood and urine screening is of little practical value, expensive, and not easily available, toxicology screening is rarely resorted to in developing countries in the initial care of the poisoned patient.


II. Routine Blood & Urine Tests: The following tests are recommended for routine screening of the overdose patient[3]:

a. Arterial blood gases.

b. Complete blood count or hemogram.

c. Electrolytes for determination of sodium, potassium, and anion gap as well as chloride, calcium, magnesium and phosphate.

d. Serum glucose.

e. Blood urea nitrogen (BUN) and creatinine for evaluation of renal function.

f. Serum osmolality and calculation of the osmolar gap.

g. Hepatic transaminases and hepatic function tests including coagulation profiles.

h. Urinalysis to check for crystalluria, hemoglobinuria or myoglobinuria.

i. Pregnancy test (females of childbearing age).


III. Radiography: Routine chest radiographs may be indicated to evaluate potential adverse effects of toxins, such as pulmonary injury due to inhalation of a toxin, aspiration of a hydrocarbon, aspiration pneumonitis or development of pulmonary edema. Abdominal x-rays may reveal radiopaque tablets, drug-filled condoms or other toxic material[4].


IV. Endoscopy: Upper GI endoscopy is indicated in irritant poisons and caustic injuries to evaluate the extent of mucosal lesions and to guide further management[1].


V. Echocardiography: Routine ECHO is indicated in toxins that cause myocardial suppression such as aluminium sulphide or endosulphan and is also useful to guide fluid and vasopressor use in hemodynamically unstable patients.

Other diagnostic studies including further laboratory investigations, ultrasonography, CT scans, MRI, etc., may be used as necessary and are also helpful in ruling out other acute or chronic conditions in an obtunded or comatose patient.

Antidote Administration

Antidotes play an important role in the management of most toxins and are essentially life saving when used as early as possible in the treatment of toxins with known antidotes[2]. However, while the judicious use of certain antidotes (eg, N-acetylcysteine, naloxone, pyridoxine) is critically important in the management of select poisoned patients, other antidotes do not necessarily offer a distinct clinical advantage and may create additional problems (eg, flumazenil, physostigmine). Therefore, antidote administration should be based on the risks versus benefits of such administration.

Enhanced Elimination

Urinary Alkalinization

Urinary alkalinization through parenteral administration of sodium bicarbonate enhances the elimination of weak acids, such as salicylates, phenobarbital, chlorophenoxy herbicides, etc., by trapping the weak acids in renal tubular fluid to prevent tubular absorption and promote urinary excretion. It also helps protect the kidneys during myoglobinuria from rhabdomyolysis. [4]

Dosing recommendations depend on the acid-base status of the patient. Initially, correction is indicated with intravenous administration of 1-2 mEq/kg of sodium bicarbonate, and then continually titrated over 4-8 hours to maintain the urinary pH between 7.5-8.0. Systemic pH should be kept below 7.55 to prevent complications of alkalemia. Complications include volume overload and metabolic alkalosis. [4]


Forced Diuresis

This is done to produce diuresis by volume expansion with Na-containing solutions, normal saline, or lactated Ringer’s solution; often combined with diuretics. It is not normally recommended except to protect the kidneys from myoglobinuria during extensive rhabdomyolysis. Complications include volume overload and electrolyte disturbances[4].


Extracorporeal Removal

a) Peritoneal Dialysis: Enhances the elimination of water-soluble, low-molecular-weight, poorly protein-bound substances with low volumes of distribution. However, this is too slow to be useful and therefore not recommended[4].


b) Hemodialysis: Hemodialysis is the primary extracorporeal method for increasing the elimination of almost all water-soluble, very low-molecular-weight, non-protein-bound compounds with low volumes of distribution and low endogenous renal clearance rates (less than 4 mL/kg/min). This is indicated in potassium, salicylates, all alcohols (ethylene glycol, methanol, isopropanol), and chloral hydrate and its primary metabolite, trichloroethanol. Complications include bleeding, access related complications, air embolism, and nosocomial infections[4].


c) Charcoal Hemoperfusion: Enhances the elimination of compounds adsorbed by AC in an extracorporeal fashion and can be used in series with hemodialysis. This is indicated in toxic doses of anticonvulsants such as carbamazepine, phenobarbital, and phenytoin; theophylline, etc. Complications are the same as dialysis and also include charcoal embolization, leukopenia, thrombocytopenia, and hypocalcemia[4].


d) Continuous Hemofiltration: Enhances the elimination of very high-molecular-weight compounds using the patient’s own arterial pressure (continuous arteriovenous hemofiltration) or a blood pump (continuous venovenous hemofiltration) to continuously perfuse a large pore size dialysis membrane. Very large molecules like methotrexate, heparin, protamine, insulin, myoglobin, and antibiotics, especially vancomycin can be eliminated using this method. Complications include the same as hemodialysis and also secondary to anticoagulation; removal of beneficial therapeutic drugs like antibiotics, antidotes, and vitamins[4].


e) Plasmapheresis: This enhances the elimination of large molecular-weight, protein-bound molecules that are not dialyzable and have limited endogenous metabolism. Fresh frozen plasma (FFP), albumin, and crystalloids are used to replace removed plasma. This is very useful in removal of Ag/Ab complexes and also certain toxins like paraquat and Amanita toxins. Complications include transfusion-related anaphylaxis or allergic manifestations[1] [4].


f) Exchange Transfusion: This is similar to plasmapheresis, but the replacement of removed blood is with packed red blood cells (PRBCs). This is usually reserved for neonates in whom dialysis or hemoperfusion may be technically difficult or impossible and MDAC and anticoagulation may be hazardous with the risks of necrotizing enterocolitis or intracerebral bleeding and therefore contraindicated. Complications of exchange transfusions are all transfusion related[1] [4].