start labetalol infusion and bolus.You can also start sodium nitroprusside if not controlled by these measures.But you didn't give gcs score ,so rule out stroke by doing CT if possible.higher Antibiotics.Also patient is developed AKI so manage volume and electrolytes and be ready for dialysis if urine output decreased and hyperkalemia or acidosis is not controlled.
Overall management 1) Continue atropine till adequate atropinization ( drying of secretions, just dilation of pupils wouldn't sufficient. It might takes days, however over atropinization should be recognised and must be avoided ( cause worsening of neurological status) 2) Ventilate patient safely with lung protective Ventilation ( avoid Ventilation associated injuries) 3) Prevent hospital acquired infections, specially VAP. Early enteral feeding. 4) Initial empiric selection of antibiotics would be based on, Severity of infection, patient's condition, risk factor for multi drug resistance organisms, local antibiogram (on our case at this stage appear to be less chances of multi drugs resistant organism infections. There is no role of prophylactic antibiotics 5) Adequate intravascular volume and hemodynamic optimization. You may assess intravascular volume conventionally by CVP but echo would be better. 6) AKI could be multi factorial but pre renal appears to be predominate cause. So hemodynamic optimization would definitively help to resolve AKI 7) Daily sedation interruption and attempt for wardening 8) If multiple attempts of weaning fail or successfully weaned but not extubatable til 6-10 days consider tracheostomy. 9) All such direct mortality from poisoning is 0%.
A case of Organophosphorus poisoning.a very common pesticide & insecticide. It causes inhibition of AChE leading to accumulation of ACh at nicotinic & muscarinic receptors, resulting in excessive cholinergic stimulation.these are hepatically metabolised. In severe poisoning, symptoms occur usually within 6 hours of exposure & unlikely to occur if the exposed person remains symptom free for 12 hours or more. Now coming to case, most of the treatment required has already been done. that is ABC,decontamination,Atropinisation,PAM. continue with this. But ,Patient is in AKI . watch out for hourly urine output, hyperkalaemia, arrhythmias, metabolic acidosis. do frequent rft check,ABG for metabolic acidosis & hyperkalaemia. treat hyperkalaemia aggressively with Inj Calcium gluconate,GI drip, sodabicarb can be given if severe metabolic acidosis present.if refractory to treatment , go for HD even if the urine output is adequate because severe hyperkalaemia disposes the patient to very high risk of Fatal ventricular arrhythmias & because of severe metabolic acidosis, the patient can land anytime in cardiac arrest. If no requirement of immediate HD hydrate the patient depending upon cardiac status (sis cvp). do echo for assessment. can continue PAM infusion till the patient remains symptom free for at least 12 hours without additional doses of atropine or until patient is extubated. also the WBC are raised, so treat with antibiotics according to creatinine clearance & also do Blood c/s & urine analysis.
already u have done adequate measures sir..continue to monitor pulse ,BP, Puipil charts and I/o chart..control seizures and neurological manifestations..Atropine and P2AM infusion..with higher antibiotics..
we should avoid diuretics in case of poisoning unless until specificly indicated .
Continue the same treatment if possible add a beta blocker.
sir, probably patient is in aki....a hypertensive background with profuse sweating ,vomiting and a probable stomach wash....all would have created a hypovolemic state and I don't think lasix at this stage would be appropriate....also a cardioselective betablocker would be a better choice rather than a pure venodilator or arteriodilator or a b blocker with alpha agonist activity....an early supportive dialysis and prompt management of hyperkalemia would prevent destabilisation of heart at any point which already is being whipped by our atropine
continue Pam infusion, ventilator support, inj. levitracetam 1 gm stat and 150 mg q8th hourly, antibiotic, ntg infusion, central line monitor cvp, I/o chart, bp, or chart, send lab-abg,ct brain,EEG.electrolytes, s. cholinesterase level,
Keep watch on p ancreatic enzymes also. Not very common but pancreatitis is also reported
Go for psudeocholinestres level And as RFT indicate pre renal , u need to replace volume adequetly by using NS 0.45 OR PLAIN DEXTTOSE , by measuring urine output or CVP if possible . and what about ABG???? avoid diuretucs
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a pt.2yrs old having a fever intermittent since 3-4days..presenting with dyspnoea ...spo2=71% . ..after hospitalisation repeated convulsive attack occur ...pt.react only while forcefull stimulation ...here after hospitalisation o2 therapy,iv fluid,inj ceftriaxone1gm bd,inj .amikacin 100mg bd inj gardenal inmaintanace dose,inj.histac ,nebulisation 8 hrly will given... o2 therapy omit since 5hr but pt.is still react on forcefull stimuli,excessive expectoration from mouth inspite of repeatedly sucction.... so plz give us to your expert opinion for further treatment of this child....Dr. Jahanavi Sorathiya3 Likes16 Answers
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Up -dated management in infectious diseases - Malaria Severe falciparum malaria is a medical emergency, and necessitates intensive nursing care and careful management (panel 1). In Asia, parenteral artesunate significantly reduced mortality from 22·4% to 14·7% compared with quinine (figure 4) (appendix).54 In the largest study53 so far of children hospitalised with severe falciparum malaria in Africa, artesunate significantly reduced mortality from 10·9% to 8·5% compared with quinine. Intravenous or intramuscular artesunate is thus the treatment of choice for severe malaria worldwide120 (including in patients with severe vivax and knowlesi malaria125). Artesunate has no important local or systemic adverse effects, although high cumulative doses (≥6 mg/kg per day) can temporarily suppress bone marrow. Delayed haemolysis starting a week after artesunate treatment for severe malaria has been noted in travellers (particularly those initially presenting with high parasitaemias) returning to hospitals in non-endemic countries.126 This haemolysis is probably partly caused by the loss of once-infected erythrocytes, which results from splenic pitting of parasites killed by artesunate. Panel 1 Treatment of severe malaria in adults and children •Artesunate 2·4 mg/kg by intravenous or intramuscular* injection, followed by 2·4 mg/kg at 12 h and 24 h; continue injection once daily if necessary† •Artemether 3·2 mg/kg by immediate intramuscular* injection, followed by 1·6 mg/kg daily •Quinine dihydrochloride 20 mg salt per kg infused during 4 h, followed by maintenance of 10 mg salt per kg infused during 2—8 h every 8 h (can also be given by intramuscular injection* when diluted to 60—100 mg/mL) Artesunate is the treatment of choice. Artemether should only be used if artesunate is unavailable. Quinine dihydrochloride should be given only when artesunate and artemether are unavailable. * Intramuscular injections should be given to the anterior thigh.Young children with severe malaria have lower exposure to artesunate and its main biologically active metabolite dihydroartemisinin than do older children and adults. Revised dose regimens to ensure similar drug exposures have been suggested In acute renal failure or severe metabolic acidosis, haemofiltration or hemodialysis should be started early.72 Dose reduction of artemisinin derivatives is unnecessary, even in renal failure. Prophylactic anticonvulsants are potentially dangerous; high-dose phenobarbital (20 mg/kg) doubled mortality in children with cerebral malaria—patients died mainly from respiratory arrest.130 In unconscious patients, blood glucose should be measured every 4—6 h and dextrose continuously infused to maintain concentrations higher than 4 mmol/L. Hypoglycaemia (<2·2 mmol/L) should be treated immediately with bolus glucose. Parasite counts and haematocrit concentrations should be measured every 6—12 h. Anaemia develops rapidly in severe malaria; if haematocrit falls to less than 20% (haemoglobin <70 g/L), then packed cells or whole (preferably fresh) blood should be transfused carefully. The transfusion threshold for children in Africa (where anaemia is very common and safe blood for transfusion is scarce) is a haematocrit concentration of 15% or less (haemoglobin concentrations less than 50 g/L). Renal function should be checked daily. Management of fluids is difficult, especially in adults, because the risks of overhydration (pulmonary oedema) have to be balanced against those of underhydration (exacerbation of renal impairment and tissue hypoperfusion). Large fluid boluses are harmful at all ages.68, 69 Early enteral feeding in non-intubated comatose adults can cause aspiration pneumonia, so feeding should not start until the third day of the coma.131 When the patient can take tablets reliably, a full course of artemisinin combination treatment should be given.120 Intravenous antimicrobials should be given to all children with suspected severe malaria in areas of moderate or high transmission.132 Convulsions should be treated with intravenous or rectal benzodiazepines and respiratory support provided when necessary. Aspiration pneumonia should be suspected in any unconscious child or adult patient with convulsions, particularly when persistent hyperventilation is noted. Hypoglycaemia or septicaemia should be suspected after sudden deterioration for no obvious reason during treatment. Patients who bleed spontaneously should be given packed red blood cells with fresh frozen plasma or, when unavailable, fresh blood and parenteral vitamin K. Uncomplicated falciparum malaria Artemisinin combination treatment is the recommended first-line therapy for uncomplicated falciparum malaria in all endemic areas, and is highly efficacious against the other human malarias. The artemisinin component (artesunate, artemether, or dihydroartemisinin) is given for 3 days with a slowly eliminated antimalarial, preferably in a fixed-dose combination (table). Artemisinin combination treatment is rapidly and reliably effective, associated with few adverse effects,133 and curative in more than 90% of cases (except in foci of artemisinin resistance). The price of such treatment has dropped substantially, making it more generally affordable. Unfortunately, fake or substandard antimalarials are widespread in many Asian and African countries, which compromises effectiveness, selects for resistance, and diminishes confidence in the health sector. Atovaquone—proguanil is highly effective everywhere, but seldom used in endemic areas because of the cost and propensity for high-grade resistance to emerge from single mutations in the cyt b gene. The duration of post-treatment prophylaxis after artemisinin combination treatment varies. Slowly eliminated partner drugs, such as mefloquine and piperaquine, provide 4—6 weeks’ prophylaxis, whereas reinfections after treatment with artemether—lumefantrine often emerge within a month. In low transmission areas, a single gametocytocidal dose of primaquine (0·25 mg base per kg) should be added to all artemisinin combination treatments for falciparum malaria (except for those in infants and pregnant women, in whom primaquine is not recommended) to sterilise the infection and prevent onward transmission.134 Testing for G6PD deficiency is not necessary with this dose. Patients should be monitored for vomiting for 1 h after any oral antimalarial dosing. If the patient vomits, another dose should be given. Minor adverse effects (eg, nausea, abdominal discomfort, headache, dizziness) occur frequently in malaria, and often result from the illness rather than the treatment. 3 day artemisinin combination regimens are well tolerated, although mefloquine is associated with increased rates of vomiting and dizziness. The frequency of serious adverse neuropsychiatric reactions to mefloquine is around one per 1000 patients treated in Asia but as high as one per 200 in African and white patients. All the antimalarial quinolines (ie, chloroquine, mefloquine, and quinine) exacerbate orthostatic hypotension, and are tolerated better by children than by adults (panel 2). Panel 2 Second line treatments and new drugs •Artesunate 2 mg/kg daily plus tetracycline* 4 mg/kg four times daily, doxycycline* 3 mg/kg daily, or clindamycin 10 mg/kg twice daily for 7 days •Quinine 10 mg salt per kg three times daily plus tetracycline* 4 mg/kg four times daily, doxycycline* 3 mg/kg daily, or clindamycin 10 mg/kg twice daily for 7 days •Atovaquone—proguanil 20 mg/kg—8 mg/kg daily for three days (with food) •Artesunate—pyronaridine 4 mg/kg—12 mg/kg daily for three days135, 136 * Not suitable for pregnant women or children younger than 8 years. Resistance Western Cambodia and the Thailand—Myanmar border, where artemisinin-resistant P falciparum has emerged,137, 138 are the regions of greatest concern. Resistance to both chloroquine and sulfadoxine—pyrimethamine emerged prreviously in this area, and in both cases the resistance genes spread to Africa and caused millions of deaths. Artemisinin-resistant parasites are cleared slowly from the blood after artemisinin combination treatment. Parasite clearance times exceed 3 days, and treatment failure occurs more often. Resistance to amodiaquine, sulfadoxine—pyrimethamine, and, to a lesser extent, mefloquine, limits deployment of artemisinin combinations containing these drugs in several areas. Up-to-date information about antimalarial drug resistance is available from the Worldwide Antimalarial Resistance Network. P vivax and other malarias Despite increasing resistance in P vivax, chloroquine is widely used to treat non-falciparum malarias, except in Indonesia and Papua New Guinea, where highly resistant P vivax is widespread.139 In Asia, P vivax and P falciparum often co-infect, and, in parts of southeast Asia, subsequent P vivax infection occurs in as much as 50% of patients treated for falciparum malaria.140 In view of the increasing resistance to chloroquine in P vivax, the potential for misdiagnosis and subsequent inadvertent use of chloroquine to treat falciparum malaria, and operational advantages, artemisinin combination treatment seems a good first-line treatment for all human malarias. To prevent relapses of tropical P vivax malaria, a full course of primaquine (0·5 mg base per kg daily for 14 days—so-called radical treatment) should be given (table).120 For Plasmodium ovale and temperate strains of P vivax, the primaquine dose is 0·25 mg base per kg per day. Testing for G6PD deficiency is necessary because daily primaquine causes potentially dangerous haemolysis in G6PD-deficient patients. In patients with mild variants of G6PD deficiency, weekly primaquine (0·75 mg base per kg) for 8 weeks is safer than, and probably as effective as, daily treatment. Pregnant women with vivax or ovale malaria should be given suppressive prophylaxis with chloroquine (5 mg base per kg per week) until delivery, at which point radical treatment with primaquine can be given. Control and elimination Where malaria has been reduced substantially, acquisition of immunity slows and symptomatic disease extends to older children and then to adults. Occasional epidemics can occur. This pattern, which is now noted in some parts of Africa, is similar to that reported previously in Asia and southern Europe. In areas of low seasonal transmission—eg, much of Asia, Central and South America, strengthening of control measures usually has a greater effect on P falciparum than on P vivax. Some countries—eg, Turkmenistan (2006), United Arab Emirates (2007), Morocco (2010), Armenia (2011)—have achieved elimination in the past 10 years. Others, where local transmission no longer occurs, await WHO certification—eg, Egypt (1998), Mauritius (1998), Oman (2000), Algeria (2005), Syria (2005). In some areas, despite substantial financial investment in malaria control, commensurate reductions in case numbers have not been noted. Possibly, the epidemiology of malaria in these areas was underestimated. Often, small foci of stable transmission within low transmission areas act as transmission reservoirs, and asymptomatic malaria has been underestimated substantially. Artemisinin resistance poses the greatest threat to global malaria control, and more vigorous containment and elimination measures than have been instituted in the past 6 years are needed. Radical measures to eliminate resistance foci, such as mass drug administration, might be needed. The value of active case detection is uncertain. Greater use of primaquine to prevent relapse of vivax malaria and as a gametocytocide in falciparum malaria would help with control and elimination in areas with low transmissionDr. Shashank Kumar Srivastav8 Likes15 Answers
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pl read these invest alongwith my previous question posted just now.Dr. S Kumar0 Like15 Answers
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