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Fatal Self-Poisoning with Lithium Carbonate

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Fatal Self-Poisoning with Lithium Carbonate Fatal self-poisoning with lithium carbonate M.R. Achong, b sc, mb; P.G. Fernandez, mrcp, frcp[c]; P.J. McLeod, md, frcp[c] Summary: In a fatal case of self- Lithium carbonate is used in the con¬ psychiatric care for a manic-depressive poisoning with lithium carbonate there trol of acute mania and in the preven¬ illness. For the 6 months preceding the was a progressive increase in serum tion of recurrent attacks of depression overdose her treatment consisted of 1500 lithium concentration for 48 hours and mania. The mg of lithium carbonate and 200 mg of optimum therapeutic each after ingestion of the overdose. It is serum concentration of lithium 8 to 12 chlorpromazine day. that the continuous increase hours after the last dose is between 0.7 She was alert, oriented and in no physi¬ suggested cal distress. The oral temperature was in serum lithium concentration reflects and 1.3 meq/l.1 However, the margin 36.7 °C, the heart rate 80 beats/min, the prolonged absorption of lithium from of safety is small, for adverse effects blood pressure 100/78 mm Hg and the relatively insoluble aggregates of usually occur with serum concentrations respiratory rate 20/min. There were no lithium carbonate in the gastrointestinal of more than 2 meq/l. The most com¬ abnormal physical findings. Blood urea tract. ln this case there was an mon clinical manifestations of lithium nitrogen (BUN) and serum electrolyte interval of 45 hours between ingestion intoxication are gastrointestinal (nau¬ values (Table I), chest radiograph and of the overdose and the onset of sea, and and neuro¬ electrocardiogram (ECG) were normal. vomiting diarrhea) Gastric and were central nervous aspiration lavage per¬ system depression. logic (hand tremor, sedation, ataxia, formed a wide-bore tube. A Simultaneous and convulsions and through mod¬ peritoneal dialysis weakness, coma).1'2 erate amount of particulate matter was were effective in hemodialysis Cardiac arrhythmias3 and renal dysfunc¬ recovered. After lavage a slurry of 100 g rapidly reducing the serum lithium tion45 are less common. of activated charcoal (Norit A) was in- concentration but there was little Lithium intoxication can result from stilled into the stomach. One month be¬ concomitant change in the patient's (a) accidental or deliberate ingestion of fore admission the lithium value had been level of consciousness. The terminal a large amount of or (b) 0.75 meq/l; on admission it was 3.7 meq/l. drug gradual Because of the of of event was a respiratory complication accumulation of lithium in patients re¬ history ingestion of the comatose state. doses of lithium large amounts of three drugs the patient ceiving therapeutic was admitted to the medical intensive care carbonate. The accumulation of lithium unit (MICU) for observation. may result from an increase in dose her first 2 in the MICU Resume: Un cas fatal d'autointoxication During days or a decrease in renal excretion of she remained alert and oriented. Oral le carbone de lithium par lithium due to renal dysfunction, re¬ temperature increased to 37.8 °C and a few Dans un cas fatal d'autointoxication duced sodium intake or diuretic ther¬ scattered rhonchi were heard. There were no abnormal par le carbonate de lithium nous apy. The majority of reported cases of neurologic findings. lithium intoxication fail into the second BUN and serum electrolyte values (Table avons observe une augmentation I), chest radiograph and ECG remained progressive de la concentration serique category,2,5"11 and in this situation pro- dromal and normal. Increasing serum lithium values de lithium pendant 48 heures apres gastrointestinal neurologic were noted (Fig. 1) but the adverse effects are a only ingestion de la dose toxique. Nous prominent feature. There effects observed were nausea, vomiting estknons que cette augmentation are few case reports6'12 describing the continue reflete une absorption clinical course after the ingestion of a prolongee de lithium a partir d'agregats large overdose of lithium carbonate. 15.0 de carbonate de lithium, relativement The case we report demonstrates cer¬ insolubles, situes dans le tube digestif. tain unusual features and raises many 10 Dans le cas present nous avons note questions regarding the management of un intervalle de 45 heures entre acute lithium intoxication. 1 de la dose et E I'ingestion toxique le 2 Case 3 debut de la depression du systeme report I nerveux central. Grace a I'application A 29-year-old woman presented to The simultanee d'une dialyse peritoneale Montreal General Hospital Apr. 2, 1974, et d'une hemodialyse, nous avons pu claiming to have ingested, 1 to 2 hours rapidement reduire la concentration before, about 200 tablets (60 g) of lithium de lithium, mais cette 150 tablets of CNS serique carbonate, (15 g) chlorpro¬ admission depression V death maneuvre n'a pas ete suivie d'une mazine and 30 tablets (0.9 g) of fluraze- ^ ¦¦¦?¦¦¦¦? amelioration notable du niveau de pam hydrochloride. She denied drinking 1 2 3 conscience du malade. Le stade ultime ethanol and before arrival at hospital had DAYS vomited twice. a ete une She had been hospitalized complication respiratoire 4 before with an de I'etat comateux. years intentional drug FIG. 1.Log serum lithium concentration overdose and since then had been under and time course. Table I.Fluid intake, urine output and BUN and serum electrolyte values during hospital stay Hospital day Variable 1 Fluid intake (ml) 610 2970 4850 5000 From the division of clinical pharmacology Urine output (ml) 500* 1950* 210 650 of The Montreal General Hospital BUN (mg/dl) 6 7 10 5 Reprint requests to: Dr. M.R. Achong, Serum Na (meq/l) 137 135 136 139 Division of clinical pharmacology, The Montreal Serum K (meq/l) 4.2 5.9 4.1 General Hospital, 1650 Cedar Ave., Montreal. 3.9 Que. H3G 1A4 *Underestimates: several specimens were lost in the watery feces. 868 CMA JOURNAL/APRIL 5, 1975/VOL. 112 (two episodes/day) and diarrhea (three the onset of central nervous system de¬ formed in the gastrointestinal tract. A episodes/day). Intravenous fluids were pression within 6 to 12 hours after an comparable situation may be salicylate given to supplement the oral intake. overdose of the Matthew et aP* have The first in consciousness was phenothiazines (e.g. self-poisoning; change or recovered of seen on the of about 45 chlorpromazine) benzodiazepines large quantities salicylate morning day 3, as hours after admission. At 8 am she was (e.g. flurazepam).13 in gastric lavage fluid long as 9 drowsy but rousable. By noon she was The most unusual feature of this case hours after ingestion of the overdose. comatose, with minimal response to max- was the progressive increase in serum The slow release of lithium into solu¬ imally painful stimuli and without lateral- lithium concentration for 48 hours tion from insoluble aggregates of lithi¬ izing neurologic signs. There was no after admission. There are three pos¬ um carbonate could account for con¬ clinical change in cardiac or pulmonary sible explanations for this phenomenon: tinued lithium absorption long after function. The diarrhea had decreased but (a) impaired excretion, (b) altered dis¬ the ingestion of the overdose. The only because pills had been seen in the feces for this the sulfate tribution or (c) continued absorption of support hypothesis is that pills previous evening, magnesium of an unknown nature were seen in the was administered through a nasogastric lithium. Lithium is excreted almost en¬ tube to hasten elimination of any drug tirely by the kidneys,14 and the patient's feces about 36 hours after admission. that was still in the gastrointestinal tract. renal function, as judged by the BUN Activated charcoal binds mainly to Because her clinical condition rapidly de¬ values, was always normal (Table I). the un-ionized moiety of lipid-soluble teriorated, peritoneal dialysis was started Her urine output was adequate during drugs,27 so one would not expect ac¬ at 2 pm and hemodialysis at 8 pm that the of tivated charcoal to bind lithium ions Because of the phase progressively increasing day. magnesium-sulfate- serum lithium concentration (Table I) and thereby reduce the amount of induced diarrhea and the fluid loss due but she became after lithium available for In this to intravenous fluids were in¬ oliguric dialysis absorption. dialysis, was case, activated charcoal was adminis¬ creased to 5 1 per 24 hours to maintain started. The oliguria probably re¬ fluid balance. Urine output decreased dur¬ sulted from a negative fluid balance tered for its possible benefit in binding ing dialysis but BUN and serum electro¬ during dialysis but it is possible that it any chlorpromazine or flurazepam in lyte values remained normal (Table I). reflects lithium-induced renal dysfunc¬ the gastrointestinal tract. During dialysis the serum lithium value tion. The claim by Almy and Taylor15 Another unusual feature of this case but was rapidly decreased (Fig. 1) there that manic patients retain more orally was the very high serum lithium con¬ no concomitant in the change patient's administered lithium during the active centration; a peak of 14 meq/l was level of consciousness. not 4 comatose but manic phase than normals is sup¬ recorded (Fig. 1). The highest serum On day she remained the work of other lithium value was more responsive to painful stimuli. ported by investiga¬ recorded in previously Her serum lithium value had decreased tors.16 Inhibition of renal excretion of reported cases of lithium intoxication to less than 2 meq/l (Fig. 1) and hemo¬ lithium by chlorpromazine seems un¬ was about 7 meq/l.9 The lack of corre¬ dialysis was discontinued at noon. Peri¬ likely because chlorpromazine induces lation between both the increasing and toneal dialysis was continued because she a very small increase in lithium excre¬ decreasing serum lithium concentration was still oliguric (Table I).
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