Severe hypoxia and hypothermia following barbiturate poisoning.
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Biomedical subjects
Publications and source records attributed to P Mahieu.
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We report two patients in whom acute arsenic poisoning was associated with a very peculiar increase in hepatocytic mitotic activity. The recognition of such an unusual picture which is likely to be related to the mitogenic properties of arsenic may be of help in the identification of acute arsenic intoxication, a life-threatening condition which is difficult to diagnose.
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The oral administration of non-steroidal anti-inflammatory drugs (NSAID) to animals induces a quick increase in intestinal permeability and secondary inflammatory lesions of the intestine. The mechanisms leading to the inflammatory lesions are hypothetical. The increased intestinal permeability could allow a greater mucosal and systemic penetration of fed antigens and bacterial products leading to an abnormal mucosal and systemic immune and inflammatory response toward these materials. We examined the effect of oral dosing with indomethacin on ovalbumin serum levels and the systemic immune response to ovalbumin in mice fed with ovalbumin. The ovalbumin serum level was higher in indomethacin-treated mice and the increase was proportional to the dose of indomethacin. It was associated with epithelial and subepithelial lesions. Moreover, the systemic humoral and, to a lesser extent, the cellular tolerance were partially abrogated in the treated mice. These findings suggest that the oral administration of indomethacin in mice induces an increased passage of fed antigen through the intestinal epithelium associated with a decrease in systemic tolerance to this antigen. The reason for this decrease remains unclear. Besides a disequilibrium between systemic and mucosal immune responses, a loss of integrity of the intestinal epithelial cells and a direct immunomodulating effect of indomethacin may also be involved. This decrease in systemic tolerance to luminal antigen could be involved in the development of NSAID enteropathy.
CASE REPORT: We report a suicidal attempt by intracardiac injection of T-61, a veterinary euthanasia drug containing embutramide, mebezonium and tetracaine in dimethylformamide. The main complications were reversible acute renal failure and pericardial effusion. There was a delayed abnormality of the liver function tests possibly related to the dimethylformamide solvent. A liver biopsy on day 16 showed a normal hepatic architecture with lipid-containing lysosomes and prominent vesicular endoplasmic reticulum noted on electron microscopy.
CASE REPORT: An 86-year-old woman accidentally ingested a preparation containing zinc and copper sulfate. At ninety minutes after ingestion, the peak plasma concentration was 1979 micrograms/dL for zinc and 209 micrograms/dL for copper, suggesting preferential absorption of zinc. The major complications were gastric and bronchial inflammation due to the corrosive properties of these compounds. Systemic manifestations also developed with cardiovascular failure and renal insufficiency, but the patient made a complete recovery. In addition to symptomatic treatment, chelation therapy with dimercaprol and D-penicillamine was given for 48 h. CONCLUSION: The available clinical and toxicokinetic data do not support the benefits of chelation in addition to supportive therapy.
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From 1975 to 1993, our University Hospital performed 2789 graft procedures. During the same period, 12 poisoned, "brain-dead" patients were considered as organ donors. The toxic substances involved were: methaqualone (n = 1), benzodiazepine alone (n = 1), benzodiazepine plus tricyclic antidepressants (n =1), tricyclic antidepressants alone (n = 1), barbiturates (n = 2), insulin (n = 2), carbon monoxide (n = 1), cyanide (n = 1), methanol (n = 1), and acetaminophen (n = 1). From these intoxicated persons, 32 organ transplants were obtained, but only 23 could be followed for 1 month and only 20 for 1 year. The outcome at 1 month was favorable in 20 of the 23 patients. Two heart transplant patients died with 24h after grafting from stroke and acute heart failure, respectively. Preoperative hepatic encephalopathy was not corrected after grafting and was directly responsible for the death of a liver transplant patient. After 1 year, 15 of the 20 recipients were still alive. Chronic hepatic graft rejection led to a fatal outcome in one recipient and to second grafting in another. Finally, one recipient died from delayed neoplasia. Based on our experience, organ procurement may be considered in a few select cases of acute poisoning. Attention should, however, be drawn to possible graft damage due to some poisons.
In Crohn's disease, the activity of the disease is difficult to evaluate and the evolution of the disease is difficult to predict. The soluble interleukin-2 receptor serum level has been reported to correlate with clinical activity of the disease and with mucosal immune activation. We compared serum soluble interleukin-2 receptor to classical inflammatory markers and other immune parameters in the assessment of clinical disease activity and prediction of relapse in patients with Crohn's disease. Soluble interleukin-2 receptor serum levels correlated well with the Crohn's disease activity index, and multivariate analysis showed that this correlation was independent of the other inflammatory and immune markers. The correlation was not greater, However, than that between some inflammatory markers, such as ESR, and Crohn's disease activity index. Longitudinal follow-up showed that a high soluble interleukin-2 receptor serum level was highly predictive of relapse. Multivariate analysis showed that the soluble interleukin-2 recepteur serum level was complementary to other inflammatory and clinical markers in the prediction of relapse of disease. We conclude that soluble interleukin-2 receptor is of use in monitoring Crohn's disease, particularly in prediction of relapse.
Dextropropoxyphene overdose may be complicated by serious cardiovascular manifestations, including conduction abnormalities and collapse. We report two patients in whom cardiac toxicity developed. Cardiovascular depression seemed to be improved after naloxone infusion in these two cases. Possible mechanisms are briefly discussed.
Acute doxorubicin-loaded nanoparticle (DXNP) renal toxicity was explored in both normal rats and rats with experimental glomerulonephritis. In normal rats, 2/6 rats given free doxorubicin (DX) (5 mg/kg) died within one week, whereas all control animals and all rats having received free NP or DXNP survived. A 3 times higher proteinuria appeared in animals treated with DXNP than in those treated with DX. Free NP did not provoke any proteinuria. Two hr post-injection, DXNP was 2.7 times more concentrated in kidneys than free DX (p < 0.025). In rats with immune experimental glomerulonephritis, 5/6 rats given DX died within 7 days, in contrast to animals treated by DXNP, NP, or untreated, which all survived. Proteinuria appeared in all series, but was 2-5 times more intense (p > 0.001) and prolonged after doxorubicin treatment (400-700 mg/day), without significant difference between DXNP and DX. Rats treated by unloaded NP behaved as controls. These results demonstrate that, in these experimental conditions, DXNP killed less animals than free DX, despite of an enhanced renal toxicity of the former. Both effects (better survival and nephrosis) are most probably related to an enhanced capture of DXNP by cells of the mononuclear phagocyte system, including mesangial cells.
The aim of our study was to determine the effect of a rectocolonic preimmunization with ovalbumin on the systemic immune response induced by a subsequent subcutaneous injection of this antigen in Balb/c mice. One rectocolonic, but not intragastric, administration of 25 mg of ovalbumin induced a detectable increase in serum anti-ovalbumin antibody level. The level reached was however much lower than after subcutaneous injection. Both intragastric and rectocolonic immunization with ovalbumin induced specific systemic cellular tolerance. However, after rectocolonic, but not intragastric, preimmunization there was no systemic humoral tolerance to this antigen. These differences in systemic immune responses after rectocolonic or intragastric administration of ovalbumin could be due to different stimulation of the systemic immune system or to differences between the colonic and small bowel mucosal immune system, which remain to be elucidated.
Refractory status epilepticus was observed in two patients who underwent vestibular neurectomy. We investigated the relationship with the use of an aluminum containing bone cement during the procedure. Two patients developed focal and thereafter generalized seizures in the late postoperative period of vestibular neurectomy (respectively after 42 and 35 days). A cement (1 g aluminum-calcium fluorosilicate) was used during the procedure to bridge bone defects. Both patients presented cerebrospinal fluid fistula. Investigations excluded common etiologies, in particular infections, and a toxic origin was suspected. Aluminum concentration was determined repeatedly in serum urine, cerebrospinal fluid and retroauricular fistula. The highest aluminum values were respectively in case 1 and 2, 112 and 63 micrograms/L for the cerebrospinal fluid, 495 and 1440 micrograms/L for the fistula, 4.4 and 4.4 micrograms/L in serum. Desferrioxamine was used as chelating agent and aluminum elimination was analyzed in the urine. Status epilepticus became refractory to intensive care therapy. The patients never recovered normal consciousness. Case 1 died 143 days after the procedure and case 2 at 80 days from brain failure. Brain post-mortem examination was obtained in Case 2. Brain aluminum concentration was 2.5 micrograms/g (wet weight) (0.85 micrograms/g in a control non exposed cadaver). The cement (0.2 g) was incubated in vitro (16 h-37 degrees C) with the cerebrospinal fluid of a control patient (cerebrospinal fluid aluminum 8 micrograms/L): aluminum concentration reached 2750 micrograms/L. A close contact between an aluminum containing cement and the cerebrospinal fluid may have resulted in encephalopathy and fatal status epilepticus in these two patients.
Experience with organ procurement from poisoned donors in brain death status is still limited in comparison with other etiologies. From 1963 to 1993, 2769 grafts (heart 141, kidney 1922, liver 623, pancreas 43) were performed in our University Hospital. Since 1975, among 1174 patients admitted to the ICU for acute poisoning, 12 patients who developed brain death status were considered for organ donation. The toxics involved were: methaqualone (1), benzodiazepines (1), benzodiazepines plus tricyclic antidepressants (2), barbiturates (2), insulin (2), carbon monoxide (1), cyanide (1), methanol (1), and acetaminophen (1). Exclusion criteria for organ removal were applied according to the nature of the toxin and the general criteria used for organ donation. The organs removed were: heart 5, heart valves for graft bank 2, kidneys 22, liver 4, pancreas 2, pancrease islet cells 2. Pertinent follow-up was obtained in 23 of 32 recipients. Immediate outcome was favorable in 20/23 patients (85%). Three patients died either from stroke, heart failure or preexisting encephalopathy. Two patients died from either chronic hepatic or renal graft rejection. None of these events could be directly related to a toxic origin. The one year survival rate of 75% is similar to that observed in the population who received organs from nonpoisoned donors. Organ procurement can be considered in few selected cases of acute poisoning. The accuracy of the diagnosis of irreversible brain damage is essential in this setting.
This case report concerns a 30-year-old man who survived a 4.2 g diltiazem overdose. He sustained vasoplegic shock with a junctional escape rhythm which required high doses of norepinephrine and epinephrine. Among other complications, ileus with paralytic intestinal pseudo-obstruction developed on day three. Cecal distention was demonstrated by abdomen computed tomodensitometry. The ileus resolved on day seven following the poisoning. Diltiazem plasma concentrations were determined during the first three days. The possible role of other medications, activated charcoal and sufentanil, is noted.
We observed a fatal case of cardiac tumor obstructing the left atrium. Death occurred after massive hemoptysis. At autopsy, the histological diagnosis was primary cardiac osteosarcoma with metastases in the adrenal gland.