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Biomedical subjects

J M Saissy

Publications and source records attributed to J M Saissy.

At least 19 recordsLinked to original sources
PubMed2002

Tachycardia and convulsions induced by accidental intravascular ropivacaine injection during sciatic block.

Ropivacaine, a recently introduced local anesthetic of the amide family (1), seems to show less toxicity than bupivacaine (2-4). Nevertheless, both neurologic and cardiovascular toxicities are possible. Six cases of ropivacaine-induced convulsions have previously been reported (5-10), of which three cases also showed cardiovascular toxicity. In three cases, total plasma concentrations were measured (Table 1).

Adult↗
PubMed1999

Oxaliplatin-induced haemolytic anaemia.

A case of haemolytic anaemia after therapy with oxaliplatin, an anticancer chemotherapeutic agent, was investigated. Haemolytic anaemia has been associated with cisplatin and carboplatin, two related drugs, but not with oxaliplatin.

Adenocarcinoma↗
PubMed1992

[Severe acute asthma in adults in black Africa].

A prospective study has been conducted in an intensive care unit of West Africa in order to determine the clinical and laboratory features of severe acute asthma in black Africans. The study concerned 55 episodes of severe acute asthma, with PaCO2 above 45 mmHg, in 42 patients (26 men and 16 women, mean age 35 +/- 3 years). A triggering factor was found in only 36 percent of the cases. None of the patients were using beta-adrenergic stimulants as maintenance therapy. The mean duration of asthmatic attacks prior to hospitalization was 49 +/- 7 hours. Three patients had cardiorespiratory arrest on admission. Mechanical ventilation was necessary on 12 occasions (initially in 4 and secondarily in 8). Four patients died. It would appear from this study that severe acute asthma in black Africans is characterized by a prolonged onset and by a frequent need for mechanical ventilation, suggesting a physiopathological mechanism different from that described in industrialized countries.

Acute Disease↗
PubMed1992

Treatment of severe tetanus by intrathecal injections of baclofen without artificial ventilation.

A study was conducted to evaluate repeated intrathecal injections of baclofen, without artificial ventilation, in the treatment of severe tetanus. Ten patients, 5 men and 5 women, with a mean age of 34 +/- 7 years, were included in the study. The dose of baclofen injected was 1000 micrograms between the ages of 16 and 55 years, 800 micrograms over the age of 55 years and 500 micrograms under the age of 16 years. The efficacy was assessed on the basis of the resolution of contractures and paroxysms and the initial dose was reinjected prior to the reappearance of these symptoms. Treatment was discontinued in the case of central nervous system depression or inefficacy. The first injection was effective in 9 cases for 24-48 h. The haemodynamic safety was always good. Five patients developed central depression with coma and respiratory depression, requiring artificial ventilation in 3 cases and reversed by flumazenil in 2 cases. Five patients were treated exclusively with baclofen with 4 cures. Five patients had to be ventilated with only one cure. This study confirms earlier studies concerning the efficacy of intrathecal baclofen in tetanus. However, the frequency of episodes of respiratory depression prevents the recommendation of repeated injections when respiratory intensive care facilities are not available.

Adolescent↗
PubMed1992

[Effects of diazepam and incidence of hypoxemia during acute chloroquine poisoning].

The effects of diazepam and the incidence of hypoxaemia on the course of acute chloroquine poisoning were studied prospectively in 21 patients. Were excluded patients who had ingested more than one drug or who had major symptoms on admission (systolic blood pressure less than 80 mmHg; QRS greater than 0.12 s; cardiac dysrhythmias, respiratory disturbances). Arterial blood gases were measured on admission (T0) and 15 min after 0.5 mg.kg-1 of diazepam had been given (T1). Gastric lavage was carried out as soon as the results of the blood gases had been obtained, and after treatment of hypoxaemia (PaO2 less than 90 mmHg). An infusion of diazepam (1 mg.kg-1.day-1) was then given. Arterial blood gases were measured after 1 (T2), 6 (T3), 12 (T4) and 24 h (T5). Hypoxaemia was present on admission in four patients who had a PaO2 = 75 +/- 10 mmHg (Pa(sys) = 130 +/- 19 mmHg; blood chloroquine concentration = 8.2 +/- 5.2 mumol.l-1; kaliemia = 3.1 +/- 0.3 mmol.l-1; PaCO2 = 35 +/- 1 mmHg). In two patients, hypoxaemia decreased after the initial dose of diazepam (T1); however, oxygen was still required by the other two at that time. Oxygen was no longer needed by any patient at T2, as all the blood gas values had returned to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1992

[Effects of diazepam on mortality from acute chloroquine poisoning].

A retrospective study was carried out, over a twelve-year period, of all cases of acute chloroquine poisoning where more than 2 g of chloroquine had been taken. It included 386 patients; of these, 60 who had taken drugs other than chloroquine, and 17 who had ingested less than 1 g of the drug, were excluded. The remaining 309 patients were allocated to two groups: a "control group", consisting of the patients admitted between January 1973 and April 1980 (n = 146), and a "diazepam group", made up of those admitted from May 1980 to December 1989 (n = 163). The patients in the latter group had had the same symptomatic treatment as those in the control group, and had been routinely given a 0.5 mg.kg-1 bolus of diazepam on admission followed by 0.1 mg.kg-1.day-1 for every 100 mg of chloroquine supposed to have been ingested. Both groups were divided into three subgroups, those patients with cardiorespiratory arrest, and those with, and those without, symptoms on admission. No statistically significant difference was found between either the control and diazepam groups or between subgroups, concerning the distribution of age, sex, amount of chloroquine supposed to have been ingested, delay in hospital admission and death rate. However, there was a higher death rate in the asymptomatic subgroup not treated with diazepam than in the diazepam group. Therefore, the routine use of diazepam for the treatment of acute chloroquine poisoning does not seem to be justified in symptomatic cases and in those with inaugural cardiac arrest.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1991

[Cerebral malaria in non-immune subjects. Current aspects in African endemic areas].

The current clinical and therapeutic aspects of cerebral malaria in non-immune adult subjects living in endemic areas of Africa were evaluated in 10 men (mean age: 40 +/- 11.4 years). On admission, 8 patients had fever, 3 were truly comatose with a Glasgow score of 7 or more. All had negative central venous pressure and only one was in a state of hyperkinetic shock. Respiratory symptoms were present in 8 cases, and jaundice was observed in 8 cases. Three patients has a haemoglobin level lower than 8 g/100 ml, and 8 had thrombocytopenia. Blood creatinine levels above 240 mumol/l and blood bilirubin levels above 50 mumol/l were found in 6 and 8 patients respectively. Plasma creatine phosphokinase was above 500 IU/l in 7 cases, and PaO2 was below 70 mmHg in 7 cases. All patients received quinine, combined with doxycycline in 6 cases. Infectious complications occurred in 5 patients, with 2 septic shocks. Two patients developed acute pulmonary oedema. Five patients died. This study shows that cerebral malaria in non-immune subjects living in endemic areas produces multivisceral deficiency similar to that observed in imported malaria. Its prognosis can be improved by loading doses of quinine and by a better prevention of nosocomial infections.

Acute Kidney Injury↗
PubMed1991

[Heroin-induced acute rhabdomyolysis].

A 24 year ald-man, was admitted in intensive care with coma and shock, 4 hours after intravenous injection of heroin. Awakening was obtained by naloxone. Diagnosis of acute rhabdomyolysis associated with heroin addiction was asserted by association of anury, hyperkalemia, and CPK increase. Recovery was obtained with, however, neurologic after-effects. Pathophysiology of acute rhabdomyolysis associated with heroin addict is obscure. Hypotheses for the cause of the muscle damage include the effects of toxicity (either directly or immunologically mediated) of the drug or an adulterant. However prolonged coma and immobilization in one position with either direct compression of the muscles or occlusions of the regional vascular supply can play a major role.

Acute Disease↗