By E. Murat. Jacksonville State University. 2018.


However generic keflex 750 mg on line, these risks must be balanced with the risks of aggravation of the epilepsy buy keflex 500mg without a prescription, ensuing seizure-induced cerebral damage and other injury if the patient is not treated keflex 750 mg on-line. The effective dose must be reached progressively and symptoms and drug tolerance evaluated every 15 to 20 days. The rate of dose reduction varies according to the length of treatment; the longer the treatment period, the longer the reduction period (see Iatrogenic causes). In the same way, a change from one antiepileptic drug to another must be made progressively with an overlap period of a few weeks. Adults: initial dose of 600 mg/day in 2 divided doses; increase by 200 mg/day every 3 days until the optimal dose for the individual has been reached (usually 1 to 2 g/day in 2 divided doses). Adults: initial dose of 200 mg/day in 1 or 2 divided doses; increase by 200 mg every week until the optimal dose for the individual has been reached (usually 800 to 1200 mg/day in 2 to 4 divided doses). Then infuse 1 g/hour, continue magnesium sulfate for 24 hours following delivery or the last seizure. Before each injection, verify the concentration written on the ampoules: it comes in different concentrations. Always have calcium gluconate ready to reverse the effects of magnesium sulfate in the event of toxicity. Other causes During pregnancy, consider that seizures may also be caused by cerebral malaria or meningitis; the incidence of these diseases is increased in pregnant women. Blood glucose levels should be measured whenever possible in patients presenting symptoms of hypoglycaemia. If hypoglycaemia is suspected but blood glucose measurement is not available, glucose (or another available sugar) should be given empirically. Always consider hypoglycaemia in patients presenting impaired consciousness (lethargy, coma) or seizures. Clinical features Rapid onset of non-specific signs, mild to severe depending on the degree of the hypoglycaemia: sensation of hunger and fatigue, tremors, tachycardia, pallor, sweats, anxiety, blurred vision, difficulty speaking, confusion, convulsions, lethargy, coma. Diagnosis Capillary blood glucose concentration (reagent strip test): – Non-diabetic patients: • Hypoglycaemia: < 60 mg/dl (< 3. Symptomatic treatment – Conscious patients: Children: a teaspoon of powdered sugar in a few ml of water or 50 ml of fruit juice, maternal or therapeutic milk or 10 ml/kg of 10% glucose by oral route or nasogastric tube. Adults: 15 to 20 g of sugar (3 or 4 cubes) or sugar water, fruit juice, soda, etc. If there is no clinical improvement, differential diagnoses should be considered: e. If patient does not return to full alertness after an episode of severe hypoglycaemia, monitor blood glucose levels regularly. Treat the cause – Other than diabetes: • Treat severe malnutrition, neonatal sepsis, severe malaria, acute alcohol intoxication, etc. Record the temperature as measured and if taken using the rectal or axillary route. In a febrile patient, first look for signs of serious illness then, try to establish a diagnosis. There is an increased risk of severe bacterial infectiona if the rectal temperature is ≥ 38°C in children 0 to 2 months; ≥ 38. Signs of severity – Severe tachycardia, tachypnoea, respiratory distress, oxygen saturation ≤ 90%. Infectious causes of fever according to localizing symptoms Signs or symptoms Possible aetiology Meningeal signs, seizures Meningitis/meningoencephalitis/severe malaria Abdominal pain or peritoneal signs Appendicitis/peritonitis/typhoid fever Diarrhoea, vomiting Gastroenteritis/typhoid fever Jaundice, enlarged liver Viral hepatitis Cough Pneumonia/measles/tuberculosis if persistent Ear pain, red tympanic membrane Otitis media Sore throat, enlarged lymph nodes Streptococcal pharyngitis, diphtheria Dysuria, urinary frequency, back pain Urinary tract infection Red, warm, painful skin Erysipelas, cellulitis, abscess Limp, difficulty walking Osteomyelitis/septic arthritis Rash Measles/dengue/haemorrhagic fever/Chikungunya Bleeding (petechiae, epistaxis, etc. Do not wrap children in wet towels or cloths (not effective, increases discomfort, risk of hypothermia). It is expressed differently by each patient depending on cultural background, age, etc. It is a highly subjective experience meaning that only the individual is able to assess his/her level of pain. Regular assessment of the intensity of pain is indispensable in establishing effective treatment. Synthesis The synthesis of information gathered during history taking and clinical examination allows aetiological diagnosis and orients treatment. It is important to distinguish: – Nociceptive pain: it presents most often as acute pain and the cause-effect relationship is usually obvious (e. On a background of constant, more or less localized pain, such as paraesthesia or burning, there are recurrent acute attacks such as electric shock-like pain, frequently associated with disordered sensation (anaesthesia, hypo or hyperaesthesia). Treatment is symptomatic only in other cases (no cause found, non-curable disease). The treatment of pain is based on a few fundamental concepts: – Pain can only be treated correctly if it is correctly evaluated. Its adverse effects have often been exaggerated and should not be an obstacle to its use. A laxative should be prescribed if the opioid treatment continues more than 48 hours. Administer with caution, for a short period, at the lowest effective dose, and monitor the child. Neuropathic pain Commonly used analgesics are often ineffective in treating this type of pain. Given its teratogenic risk, carbamazepine should only be used in women of childbearing age when covered by non-hormonal contraception (copper intrauterine device). A multidisciplinary approach including medical treatment, physiotherapy, psychotherapy and nursing is often necessary to allow good pain relief and encourage patient self- management. Co-analgesics The combination of certain drugs may be useful or even essential in the treatment of pain: antispasmodics, muscle relaxants, anxiolytics, corticosteroids, local anaesthesia, etc. It is a frequent symptoma in tropical settings where 10 to 20% of the population present with Hb levels less than 10 g/dl. The groups most at risk are children and young women, particularly during pregnancy. Most anaemias are well tolerated and can be corrected with simple aetiological treatment. Clinical features – Common signs of anaemia: pallor of the conjunctivae, mucous membranes, palms of hands and soles of feet; fatigue, dizziness, oedema in the lower limbs, dyspnoea, tachycardia, heart murmur. Tablets of 200 mg ferrous sulphate such as those of ferrous sulphate + folic acid contain 65 mg of elemental iron. To determine the blood volume required and the rate of transfusion, see next page. If there is no possibility of screening, it is up to the physician to weigh the transfusion risk with the life or death risk of not transfusing the patient. Adults Determine the volume of whole blood to be Example: haemoglobin required = 7 g/dl transfused: patient’s haemoglobin = 4 g/dl V = (haemoglobin required minus patient’s patient’s weight = 60 kg haemoglobin) multiplied by 6 multiplied by Volume in ml = (7 – 4) x 6 x 60 = 1080 ml patient’s weight Determine the transfusion rate: Example: 1080 ml to be administered over 3 hours (1 ml of whole blood = 15 drops) 1080 (ml) ÷ 180 (minutes) = 6 ml/minute 6 (ml) x 15 (drops) = 90 drops/minute Children Newborns and children under 1 year: Example: a malnourished child weighing 25 kg 15 ml/kg over 3 to 4 hours 10 (ml) x 25 (kg) = 250 ml over 3 hours Children over 1 year: 250 (ml) ÷ 180 (minutes) = 1.

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In practical terms it would be near impossible to license non-commercial small scale production keflex 750 mg free shipping, even if some of the product was circulated amongst friends buy discount keflex 500 mg on-line. Basic guidelines could be made publicly available and limits could be placed on how much production was allowed for any individual but experience with such schemes in Europe suggests they are hard to enforce and often ignored by police and growers alike cheap 500 mg keflex with visa. A licensing model might become appropriate for small to medium sized cannabis clubs or societies of growers who share supply/exchange on a non-proft basis, so that age and quality controls could be put in place, and some degree of accountability could be established. Drugs are commonly placed into categories according to their similarities in action and/or their physiologic effect when introduced into the system. The following two sections describe the basic categories of drugs commonly used in our laboratory. While these two chapters have some detailed descriptions of drugs that are important for our laboratory, they are still useful for the non‐specialist, as they explain the specific uses of these drugs in the laboratory, and their dosages for different procedures. Anticholinergics Anticholinergic agents may be indicated prior to the administration of a variety of anesthetic and related agents, including sedatives, narcotics, barbiturates, and inhalant anesthetic agents. Atropine sulfate, scopolamine, and glycopyrrolate are the three principle anticholinergics used in the laboratory. At the neuromuscular junction, where the receptors are principally or exclusively nicotinic, extremely high doses of atropine or related drugs are required to cause any degree of blockade. However, quaternary ammonium analogs of atropine and related drugs generally exhibit a greater degree of nicotinic blocking activity and, consequently, are likely to interfere with ganglionic or neuromuscular transmission in doses that more closely approximate those that produce muscarinic block. Autoradiographic studies have revealed a widespread distribution of muscarinic receptors throughout the human brain. More recent studies using muscarinic receptor subtype‐specific antibodies demonstrate discrete localization of these subtypes within brain regions. At high or toxic doses, the central effects of atropine and related drugs generally consist of stimulation followed by depression. Parasympathetic neuroeffector junctions in different organs are not equally sensitive to the muscarinic receptor antagonists. Small doses of muscarinic receptor antagonists depress salivary and bronchial secretion and sweating. With larger doses, the pupil dilates, accommodation of the lens to near vision is inhibited, and vagal effects on the heart are blocked so that the heart rate is increased. Larger doses inhibit the parasympathetic control of the urinary bladder and gastrointestinal tract, therein inhibiting micturition and decreasing the tone and motility of the gut. Thus, doses of atropine and most related muscarinic receptor antagonists that reduce gastrointestinal tone and depress gastric secretion also almost invariably affect salivary secretion, ocular accommodation, and micturition. This hierarchy of relative sensitivities probably is not a consequence of differences in the affinity of atropine for the muscarinic receptors at these sites, because atropine does not show selectivity toward different muscarinic receptor subtypes. More likely determinants include the degree to which the functions of various end organs are regulated by parasympathetic tone and the involvement of intramural neurons and reflexes. The muscarinic receptor antagonists block the responses of the sphincter muscle of the iris and the ciliary muscle of the lens to cholinergic stimulation. The wide pupillary dilatation results in photophobia; the lens is fixed for far vision, near objects are blurred, and objects may appear smaller than they are. The normal pupillary reflex constriction to light or upon convergence of the eyes is abolished. These effects can occur after either local or systemic administration of the alkaloids. Locally applied atropine or scopolamine produces ocular effects of considerable duration; accommodation and pupillary reflexes may not fully recover for 7 to 12 days. The muscarinic receptor antagonists used as mydriatics differ from the sympathomimetic agents in that the latter cause pupillary dilatation without loss of accommodation. Muscarinic receptor antagonists administered systemically have little effect on intraocular pressure except in patients with narrow‐angle glaucoma, where the pressure may occasionally rise dangerously. The rise in pressure occurs when the anterior chamber is narrow and the iris obstructs entry of aqueous humor into the trabeculae. The drugs may precipitate a first attack in unrecognized cases of this rare condition. Atropine‐like drugs generally can be used safely in this latter condition, particularly if the patient is also adequately treated with an appropriate miotic agent. Atropine Sulfate Description: : It acts directly on the smooth muscles and secretory glands innervated by postganglionic cholinergic nerves, blocking the para‐sympathomimetic effects of acetylcholine. Usage: As a preanesthetic it is used both because of the mild respiratory stimulation because it inhibits salivary secretion. In reversing paralysis it is used in conjunction with the administration of prostigmin to block the muscarinic receptors. Administration of prostigmin without atropine can cause parasympathetic hyperactivity. Robinul Description: Glycopyrrolate, like other anticholinergic (antimuscarinic) agents, inhibits the action of acetylcholine on structures innervated by postganglionic cholinergic nerves and on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These peripheral cholinergic receptors are present in the autonomic effector cells of smooth muscle, cardiac muscle, the sinoatrial node, the atrioventricular node, exocrine glands, and, to a limited degree, in the autonomic ganglia. Thus, it diminishes the volume and free acidity of gastric secretions and controls excessive pharyngeal, tracheal, and bronchial secretions. The highly polar quaternary ammonium group of glycopyrrolate limits its passage across lipid membranes, such as the blood‐brain barrier, in contrast to atropine sulfate and scopolamine hydrobromide, which are non‐polar tertiary amines which penetrate lipid barriers easily. Peak effects occur approximately 30 to 45 minutes after intramuscular administration. The vagal blocking effects persist for 2 to 3 hours and the antisialagogue effects persist up to 7 hours, periods longer than for atropine. With intravenous injection, the onset of action is generally evident within one minute. Usage: In anesthesia: Robinul (glycopyrrolate) Injectable is indicated for use as a preoperative antimuscarinic to reduce salivary, tracheobronchial, and pharyngeal secretions; to reduce the volume and free acidity of gastric secretions; and, to block cardiac vagal inhibitory reflexes during induction of anesthesia and intubation. When indicated, Robinul Injectable may be used intraoperatively to counteract drug‐induced or vagal traction reflexes with the associated arrhythmias. Investigate any tachycardia before giving glycopyrrolate since an increase in the heart rate may occur. In case of overdosage, to combat peripheral anticholinergic effects, a quaternary ammonium anticholinesterase such as neostigmine methylsulfate (which does not cross the blood‐brain barrier) may be given intravenously in increments of 0. This dosage may be repeated every five to ten minutes until anticholinergic overactivity is reversed or up to a maximum of 2. Indication for repetitive doses of neostigmine should be based on close monitoring of the decrease in heart rate and the return of bowel sounds. In the event of a curare‐like effect on respiratory muscles, artificial respiration should be instituted and maintained until effective respiratory action returns.

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Potential role for interleukin-28B genotype in treatment decision-making in recent hepatitis C virus infection buy keflex 250 mg overnight delivery. Impact of alcohol on the histological and clinical progression of hepatitis C infection buy keflex 250 mg online. A significant sex--but not elective cesarean section--effect on mother-to-child transmission of hepatitis C virus infection order 500 mg keflex visa. Rates of postoperative complications among human immunodeficiency virus- infected women who have undergone obstetric and gynecologic surgical procedures. Because the demyelinating lesions can involve different brain regions, specific deficits vary from patient to patient. The focal or multifocal nature of the pathology is responsible for the consistency of clinical presentations with distinct focal symptoms and signs, rather than as a more diffuse encephalopathy, or isolated dementia or behavioral syndrome, all of which are uncommon without concomitant focal findings. Headache and fever are not characteristic of the disease, and when present may indicate presence of another opportunistic infection. The lesions are hyperintense (white) on T2-weighted and fluid attenuated inversion recovery sequences and hypointense (dark) on T1- weighted sequences. Although contrast enhancement is present in 10% to 15% of cases, it is usually sparse with a thin or reticulated appearance adjacent to the edge of the lesions. Sensitive assays that detect as few as 50 copies/ml are now available, with some research labs exceeding this level of sensitivity. Neurological deficits often persist, but some patients experience clinical improvement. The trial was later halted by the sponsor, because demonstration of efficacy was futile (http://clinicaltrials. No clear guidelines exist for the timing of follow-up assessments, but it is reasonable to be guided by clinical progress. Histopathology typically demonstrates perivascular mononuclear inflammatory infiltration. In the absence of comparative data, adjuvant corticosteroid therapy should be tailored to individual patients. A taper may begin with a dose of 60 mg per day in a single dose, tapered over 1 to 6 weeks. If corticosteroid therapy is initiated during pregnancy, blood sugar monitoring should be included as insulin resistance is increased during pregnancy. Progressive multifocal leukoencephalopathy revisited: Has the disease outgrown its name? Natalizumab-associated progressive multifocal leukoencephalopathy in patients with multiple sclerosis: lessons from 28 cases. A case of progressive multifocal leukoencephalopathy in a patient treated with infliximab. Predictive factors for prolonged survival in acquired immunodeficiency syndrome- associated progressive multifocal leukoencephalopathy. Inflammatory reaction in progressive multifocal leukoencephalopathy: harmful or beneficial? Spinal cord lesions of progressive multifocal leukoencephalopathy in an acquired immunodeficiency syndrome patient. Hyperintense cortical signal on magnetic resonance imaging reflects focal leukocortical encephalitis and seizure risk in progressive multifocal leukoencephalopathy. Metabolite abnormalities in progressive multifocal leukoencephalopathy by proton magnetic resonance spectroscopy. Diagnosis of progressive multifocal leukoencephalopathy by stereotactic brain biopsy utilizing immunohistochemistry and the polymerase chain reaction. Progressive multifocal leukoencephalopathy: improved survival of human immunodeficiency virus-infected patients in the protease inhibitor era. Clinical course and prognostic factors of progressive multifocal leukoencephalopathy in patients treated with highly active antiretroviral therapy. Clinical outcome of long-term survivors of progressive multifocal leukoencephalopathy. Predictors of survival and functional outcomes in natalizumab-associated progressive multifocal leukoencephalopathy. Failure of cytarabine in progressive multifocal leukoencephalopathy associated with human immunodeficiency virus infection. The atypical antipsychotic agents ziprasidone [correction of zisprasidone], risperdone and olanzapine as treatment for and prophylaxis against progressive multifocal leukoencephalopathy. Progressive multifocal leukoencephalopathy in a haploidentical stem cell transplant recipient: a clinical, neuroradiological and virological response after treatment with risperidone. Favourable outcome of progressive multifocal leucoencephalopathy in two patients with dermatomyositis. Mirtazapine use in human immunodeficiency virus-infected patients with progressive multifocal leukoencephalopathy. Topotecan in the treatment of acquired immunodeficiency syndrome-related progressive multifocal leukoencephalopathy. Progression of progressive multifocal leukoencephalopathy despite treatment with beta-interferon. Successful treatment of progressive multifocal leukoencephalopathy with low-dose interleukin-2. Nonmyeloablative allogeneic stem cell transplantation for refractory Hodgkin’s lymphoma complicated by interleukin-2 responsive progressive multifocal leukoencephalopathy. Progressive multifocal leukoencephalopathy: current treatment options and future perspectives. Neurological immune reconstitution inflammatory response: riding the tide of immune recovery. Inflammatory reactions in progressive multifocal leukoencephalopathy after highly active antiretroviral therapy. Fatal immune restoration disease in human immunodeficiency virus type 1-infected patients with progressive multifocal leukoencephalopathy: impact of antiretroviral therapy-associated immune reconstitution. Progressive multifocal leucoencephalopathy with unusual inflammatory response during antiretroviral treatment. Is maraviroc beneficial in paradoxical progressive multifocal leukoencephalopathy-immune reconstitution inflammatory syndrome management? Immune reconstitution inflammatory syndrome in a patient with progressive multifocal leukoencephalopathy. Clinical and immunologic effects of maraviroc in progressive multifocal leukoencephalopathy. In 2015, the World Health Organization estimated that 97 countries had ongoing malaria transmission, and almost half the world’s population, approximately 3.

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Strong recommendation buy keflex 750 mg low price, moderate-quality evidence Where intramuscular injections of artesunate are not available generic keflex 750mg online, treat children < 6 years with a single rectal dose (10 mg/kg bw) of artesunate generic 750mg keflex with amex, and refer immediately to an appropriate facility for further care. Strong recommendation, moderate-quality evidence Mortality from untreated severe malaria (particularly cerebral malaria) approaches 100%. With prompt, effective antimalarial treatment and supportive care, the rate falls to 10–20% overall. Within the broad defnition of severe malaria some syndromes are associated with lower mortality rates (e. The exact risk depends on the species of infecting malaria parasite, the number of systems affected, the degree of vital organ dysfunction, age, background immunity, pre-morbid, and concomitant diseases, and access to appropriate treatment. Tests such as a parasite count, haematocrit and blood glucose may all be performed immediately at the point of care, but the results of other laboratory measures, if any, may be available only after hours or days. As severe malaria is potentially fatal, any patient considered to be at increased risk should be given the beneft of the highest level of care available. The attending clinician should not worry unduly about defnitions: the severely ill patient requires immediate supportive care, and, if severe malaria is a possibility, parenteral antimalarial drug treatment should be started without delay. Severe acidosis manifests clinically as respiratory distress (rapid, deep, laboured breathing). Decompensated shock is defned as systolic blood pressure < 70 mm Hg in children or < 80 mm Hg in adults, with evidence of impaired perfusion (cool peripheries or prolonged capillary refll). Severe knowlesi malaria is defned as for falciparum malaria but with two differences: • P. Secondary objectives are prevention of disabilities and prevention of recrudescent infection. Death from severe malaria often occurs within hours of admission to a hospital or clinic, so it is essential that therapeutic concentrations of a highly effective antimalarial drug be achieved as soon as possible. Management of severe malaria comprises mainly clinical assessment of the patient, specifc antimalarial treatment, additional treatment and supportive care. An open airway should be secured in unconscious patients and breathing and circulation assessed. The patient should be weighed or body weight estimated, so that medicines, including antimalarial drugs and fuids, can be given appropriately. An intravenous cannula should be inserted, and blood glucose (rapid test), haematocrit or haemoglobin, parasitaemia and, in adults, renal function should be measured immediately. A detailed clinical examination should be conducted, including a record of the coma score. Several coma scores have been advocated: the Glasgow coma scale is suitable for adults, and the simple Blantyre modifcation is easily performed in children. Unconscious patients should undergo a lumbar puncture for cerebrospinal fuid analysis to exclude bacterial meningitis. If facilities are available, arterial or capillary blood pH and gases should be measured in patients who are unconscious, hyperventilating or in shock. Blood should be taken for cross-matching, a full blood count, a platelet count, clotting studies, blood culture and full biochemistry (if possible). Careful attention should be paid to the patient’s fuid balance in severe malaria in order to avoid over- or under-hydration. Cerebral malaria is not associated with signs of meningeal irritation (neck stiffness, photophobia or Kernig’s sign), but the patient may be opisthotonic. As untreated bacterial meningitis is almost invariably fatal, a diagnostic lumbar puncture should be performed to exclude this condition. There is also considerable clinical overlap between septicaemia, pneumonia and severe malaria, and these conditions may coexist. In malaria-endemic areas, particularly where parasitaemia is common in young age groups, it is diffcult to rule out septicaemia immediately in a shocked or severely ill obtunded child. In all such cases, empirical parenteral broad-spectrum antibiotics should be started immediately, together with antimalarial treatment. Two classes of medicine are available for parenteral treatment of severe malaria: artemisinin derivatives (artesunate or artemether) and the cinchona alkaloids (quinine and quinidine). The largest randomized clinical trials ever conducted on severe falciparum malaria showed a substantial reduction in mortality with intravenous or intramuscular artesunate as compared with parenteral quinine. The reduction in mortality was not associated with an increase in neurological sequelae in artesunate-treated survivors. The trials were conducted in various African and Asian countries between 1989 and 2010. Other considerations The guideline development group considered that the small increase in neurological sequelae at discharge after treatment with artesunate was due to the delayed recovery of the severely ill patients, who would have died had they received quinine. Although the safety of artesunate given in the frst trimester of pregnancy has not been frmly established, the guideline development group considered that the proven benefts to the mother outweigh any potential harm to the developing fetus. Strong recommendation based on pharmacokinetic modelling The dosing subgroup reviewed all available pharmacokinetic data on artesunate and the main biologically active metabolite dihydroartemisinin following administration of artesunate in severe malaria (published pharmacokinetic studies from 71 adults and 265 children). Simulations of artesunate and dihydroartemisinin exposures were conducted for each age group. The revised parenteral dose regimens are predicted to provide equivalent artesunate and dihydroartemisinin exposures across all age groups. Population pharmacokinetics of intravenous artesunate: a pooled analysis of individual data from patients with severe malaria. Artesunate is dispensed as a powder of artesunic acid, which is dissolved in sodium bicarbonate (5%) to form sodium artesunate. The solution is then diluted in approximately 5 mL of 5% dextrose and given by intravenous injection or by intramuscular injection into the anterior thigh. The solution should be prepared freshly for each administration and should not be stored. Artesunate is rapidly hydrolysed in-vivo to dihydroartemisinin, which provides the main antimalarial effect. Studies of the pharmacokinetics of parenteral artesunate in children with severe malaria suggest that they have less exposure than older children and adults to both artesunate and the biologically active metabolite dihydroartemisinin. Body weight has been identifed as a signifcant covariate in studies of the pharmacokinetics of orally and rectally administered artesunate, which suggests that young children have a larger apparent volume of distribution for both compounds and should therefore receive a slightly higher dose of parenteral artesunate to achieve exposure comparable to that of older children and adults. Between 2010 and 2012, there were six reports involving a total of 19 European travellers with severe malaria who were treated with artesunate injection and developed delayed haemolysis. In a prospective study involving African children, the same phenomenon was reported in 5 (7%) of the 72 hyperparasitaemic children studied. Artesunate rapidly kills ring-stage parasites, which are then taken out of the red cells by the spleen; these infected erythrocytes are then returned to the circulation but with a shortened life span, resulting in the observed haemolysis. Thus, post-treatment haemolysis is a predictable event related to the life-saving effect of artesunate. Hyperparasitaemic patients must be followed up carefully to identify late-onset anaemia. Artemether and artesunate have not been directly compared in randomized trials in African children.