Suicidal and Accidental Digoxin Ingestion - Circulationcirc.ahajournals.org/content/circulationaha/44/1/29.full.pdf · Suicidal and Accidental Digoxin Ingestion Report of Five Cases

Suicidal and Accidental Digoxin Ingestion

Report of Five Cases with Serum Digoxin

Level Correlations

By THOMAS W. SMITH, M.D., AND JAMES T. WII.ILSON, M.D.

SUMMARYClinical and serum digoxin concentration data are presented for five cases of acci-

dental or suicidal ingestion of large amounts of digoxin. Three patients, 20 years ofage or less, were without previous evidence of heart disease and responded with thedevelopment of atrioventricular block or sino-atrial exit block, which was reversed intwo instances by atropine. The third died with refractory hyperkalemia, suggestinggeneralized inhibition of the cellular sodium-potassium transport system. Ventricularectopic beats did not occur in any of these three. In contrast, two patients with pre-

existing advanced coronary artery disease developed multifocal ventricular prematurebeats, ventricular tachycardia, and ventricular fibrillation as initial manifestations oftoxicity.Serum digoxin levels 4 or more hours after each ingestion were markedly in excess

of those ordinarily encountered in patients receiving usual therapeutic doses, reachinglevels as high as 42 ng/ml. Apparent serum half-times between 5 and 48 hours aftereach ingestion were shorter than those usually observed with normal therapeutic dosesof digoxin.

Additional Indexing Words:Digoxin intoxication Suicide Serum

TNGESTION of large amounts of digitalisglycosides accidentally or with suicidal

intent constitutes at once a clinical emergency,a therapeutic challenge, and an unusualopportunity for observation of severe digitalisintoxication. Such cases have been reportedpreviouslyl-5 but have included very fewinstances of digoxin ingestion. No reportedcases have, to our knowledge, been studied

From the Cardiac Unit, Department of Medicine,Massachusetts General Hospital and Harvard MedicalSchool, Boston, Massachusetts.

Supported in part by Fellowship Grant FO 3HE44673 and Contract PH 43 67 1443 from the U. S.Public Health Service, and by grants from theAmerican Heart Association and Burroughs WellcomeCo. (U.S.A.).

Address for reprints: Dr. Smith, Cardiac Unit,Massachusetts General Hospital, Fruit Street, Boston,Massachusetts 02114.

Received December 18, 1970; revision accepted forpublication March 11, 1971.

Circulation, Volume XLIV, July 1971

digoxin concentration Radioimmunoassay

with measurements of serum digitalis glyco-side concentration. It is the purpose of thisreport to describe five patients who acciden-tally or suicidally ingested large amounts ofdigoxin, and in whom serial measurements ofserum digoxin concentration are available forcorrelation with the clinical course.

Methods

Detailed serial clinical observations and serialelectrocardiograms were available for each of thefive patients included in this series.

Blood was obtained for serum digoxin assay byroutine venipuncture at the times indicated intable 1. Following separation of formed elementsby centrifugation, serum was assayed in duplicatefor digoxin concentration by a sensitive andprecise radioimmunoassay method previously de-scribed.6' 7 The serum was diluted when veryhigh concentrations were encountered, in orderthat the level measured might fall on an optimallysensitive portion of the standard curve.

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SMITH, WILLERSON

Table 1

Summnary of Serum Digoxin Concentration Data

Estimated digoxin dose Time after ingestion Serum digoxin concentrationPatient (mg) (hr) (ng/ml)

1 (J.F.) 5.75 1 15.513 12.525 4.841 2.2

2 (M.B.) Uncertain 5 11.120 5.2

3 (N.M.) 23 4 42.039.5

8 25.54 (J.R.) 7.35 5 14.0

96 0.75 (N.M.) o 4 20.0

24 4.848 2.172 1.296 0.7

Case StudiesCase 1

J. F., a 22-year-old boy weighing 37 lb.,accidentally ingested 5.75 mg digoxin in theform of 0.25-mg tablets. He was given ipecacwithin approximately 30 min of the ingestion, andbrought to the hospital. There was no previoushistory of cardiac disease. On initial physicalexamination he had a blood pressure of 90/60, aregular pulse rate of 85 beats/min, and normalrespirations and temperature. The results of theremainder of the physical examination werewithin normal limits. An ECG taken on admissionshowed slight sinus arrhythmia. Four hours afteradmission, intermittent sino-atrial (SA) pausesor, more likely, SA exit block was observed, withprobable atrioventricular (A-V) junctional escapebeats. Atropine in small doses immediatelyrestored normal sinus rhythm (fig. 1). Electro-cardiograms taken 2 hr subsequently demonstrat-ed first degree A-V block followed by 2:1 seconddegree A-V block. Atropine was not given at this

time. Twenty-eight hours after admission stablefirst degree block was present, soon followed bynormal sinus rhythm.

Case 2M. B., a healthy 20-year-old woman weighing

110 lb., was admitted to the hospital 4 hr afteringesting an uncertain number of digoxin tabletswith suicidal intent.

Blood pressure on admission was 140/80, andheart rate was regular at 80 beats/min. Theresults of cardiovascular and chest examinationswere unremarkable. She remained consciousthroughout her hospital stay. An electrocardio-gram taken 6 hr after admission demonstratedsinus rhythm with first degree A-V block. Soonthereafter high grade A-V block appeared (fig.2), with ventricular rates as slow as 25beats/min. Small amounts of intravenous atropine(0.4 mg) given at this time completely eliminatedthe high grade A-V block with reversion to a sinustachycardia with normal P-R interval. On thesecond day, sinus rhythm with only first degree

Figure 1

Rhythm strips from case 1. (Left panel) Sino-atrial pauses or, more likely, exit block. Thelast two complexes probably represent A-V junctional escape beats. (Right panel) Taken10 min after intravenous injection of 0.15 mg atropine. Normal sinus rhythm at a rateof 83 beats/min.

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DIGOXIN INGESTION

1

1i

a

Figure 2

Twelve-lead electrocardiogram from case 2, taken approximately 8 hr after ingestion ofdigoxin with suicidal intent. High grade A-V block is present, which could be completelyreversed by atropine with reversion to a sinus tachycardia with normal P-R interval.

block was present. On the third hospital day, allECG evidence of digoxin excess had disappeared.

Case 3*

N. M., a 17-year-old female previously in goodhealth (weight approximately 115 lb.), enteredthe hospital 3 hr after ingesting 23 mg digoxinand 1300 mg propoxyphene hydrochloride (Dar-von) with the intention of committing suicide.She vomited an uncertain amount of the ingestedmaterial later.On admission to the hospital she appeared

lethargic, but responded to questions. Her bloodpressure was 100/60, and her pulse was 55beats/min. Her initial electrocardiogram demon-strated A-V dissociation with QRS widening,which progressed from 0.09 sec to 0.40 sec duringthe first few hours after hospital admission. Herinitial serum potassium level was 7.8 mEq/liter(range on serial determinations, 7.7 to 9.8mEq/liter); the arterial pH was 7.40. Despiteintensive efforts to control the hyperkalemia withsodium bicarbonate, glucose and insulin, and so-

dium polystyrene sulfonate (Kayexalate) therapy,she expired 33 hr after admission with an asystolicarrest. Resuscitative efforts were unsuccessful.During the resuscitation, attempted pervenous

*This case is to be separately reported in detail byDrs. P. LaRaia, C. Blum, and B. Lown.

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SMITH, WILLERSON

Figure 3

Rhythm strips from case 5, showing multifocal ven-tricular premature beats following ingestion of 200.25-mg digoxin tablets superimposed on a chronicoral maintenance dose of 0.25 mg/day.

right ventricular pacing failed to elicit anyelectrical response from the heart.

Case 4

J. R. was a 208 lb., 65-year-old man withknown coronary artery disease and two previousmyocardial infarctions. He was admitted to thehospital 2 hr after taking 7.5 mg digoxin and 18 gchlorothiazide with suicidal intent. He had beenon a chronic oral maintenance dose of digoxin of0.25 mg/day up to the time of the ingestion. Onphysical examination he had a blood pressure of100/60, pulse rate of 60 beats/min (atrialfibrillation), and a grade 2/6 apical systolicmurmur. His initial ECG demonstrated atrialfibrillation with a relatively slow ventricularresponse and evidence of old inferior andanteroseptal myocardial infarctions. Approximate-ly 3 hr after admission, recurrent runs ofventricular tachycardia and three episodes ofventricular fibrillation developed, which weremanaged with intravenous lidocaine and DCdefibrillation. Ventricular tachycardia, with ratesvarying from less than 100 beats/min ("slowventricular tachycardia") to 150 beats/min,occurred intermittently during the first 6 to 20 hrfollowing admission. Twenty-four hours after hisarrival at the hospital, A-V junctional rhythm at arate of 66 beats/min appeared. At this time theventricular ectopic beats had almost entirely

disappeared. Subsequently type I second degreeA-V block (Wenckebach block) developed,followed 1 day later by sinus rhythm with firstdegree A-V block. Three days after admission allECG evidence of digoxin excess had disappeared,and antiarrhythmic agents were uneventfullydiscontinued.

Case 5

N. M. was a 155 lb., 51-year-old white malewith a past history of severe coronary insufficien-cy. He was admitted to the hospital aftersuicidally ingesting 5 mg digoxin in the form of0.25-mg digoxin tablets. He had been hospital-ized several times previously for coronary insuffi-ciency. He had been maintained since 1968 ondigoxin (0.25 mg/day) for chronic congestiveheart failure. In April, 1969, coronary arteriog-raphy demonstrated three-vessel coronary arterydisease with severe proximal narrowing of allthree vessels. He subsequently had anterior andposterior internal mammary artery implantswithout marked influence on the frequency orseverity of his chest pain. On physical examina-tion at the time of admission he had a bloodpressure of 170/110, a regular pulse rate of 80beats/min, and normal respirations and tempera-ture. A grade 2/6 systolic ejection murmur washeard along the left sternal border; at the apex,prominent third and fourth heart sounds werenoted.

20.0

, 10.0

U 6.0> 4.0

'5 2.0c:1

Z! 1.011 A_^0.6 _

TX/2= 32 Hrs.

I-

0 20 40 60 80 100T/ME (HOURS)Figure 4

Semilogarithmic plot of serum digoxin concentrationvs. time for case 5. Values are shown over a time spanfrom 4 to 96 hr after the ingestion. Only after 48 hr,when the serum level has falen to almost the usualtherapeutic range, does the half-time reach the ex-pected value of 32 hr.


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Within 1% hr after admission, multifocalventricular ectopic beats appeared (fig. 3) withbrief runs of ventricular tachycardia respondingto intravenous lidocaine and diphenylhydantoin.A temporary pervenous pacemaker catheter was

inserted, and the demand rate was set above hisown intrinsic rate so that both "overdrive" anddrug suppression of his ventricular ectopic beatscould be used. This proved to be effective incontrolling the ventricular extrasystoles, and 24 hrlater only first degree A-V block was present.Three days after admission he was in sinusrhythm with a normal P-R interval.

Serum Digoxin ConcentrationsResults of measurements of serum digoxin

concentration in each of the five patients are

summarized in table 1. Duplicate determina-tions agreed within 5% in each instance.Semilogarithmic plots of serum concentrationsagainst time for samples drawn 5 hr or laterafter the ingestion yielded apparent half-timesfor clearance from the serum of 12, 14, 6, and22 hr for cases 1, 2, 3, and 4, respectively. Itshould be noted that the limited numbers ofserum samples available for study in cases 2,3, and 4 allow only approximations of averagehalf-times over the indicated time spans. Forcase 5, in which serum levels were measuredover a wider range of times and concentra-tions, a progressive lengthening of the appar-

ent serum half-time from 10 to 31 hr was

observed, as plotted in figure 4.

DiscussionAlthough uncommon, accidental or deliber-

ate ingestion of very large quantities ofdigoxin occurs with sufficient frequency thatwe have studied five cases in a period ofslightly over 1 year. This has provided theopportunity to observe the effect of severe

excess of digoxin on previously normal as wellas diseased hearts, and to correlate the clinicalstate with serum digoxin concentrations. Ourgeneral experience has yielded a mean serum

digoxin concentration of 1.4 0.7 (SD) ng/mlin a series of 131 adult patients on oralmaintenance digoxin without evidence oftoxicity.7 Ninety percent of these nontoxicpatients had serum levels less than 2.0 ng/ml.Among 48 hospitalized patients with cardiacdisease who showed definite evidence of


digoxin intoxication, 87% had serum levelsgreater than 2.0 ng/ml, with a mean of3.7 + 1.0 (SD). Hence the levels observed inthe patients in this study (table 1) documentthe exposure to extraordinary amounts ofdigoxin.Of the five patients reported here, all had

blood urea nitrogen or serum creatinine valuesin the normal range. Three were 20 years ofage or less and were without previousevidence of heart disease. In all three, thecardiac response to ingestion of very largedoses of digoxin was the development of heartblock: high grade A-V block in two instancesand first and second degree A-V block in thethird. Ventricular premature beats did notoccur in any of the three. Two of the threepatients survived despite very high serum, andpresumably myocardial, levels of digoxin. Inone of these patients, atropine revertedsignificant A-V block to a normal conductionpattern, and sino-atrial exit block was reversedin the other. Thus, despite the well-knownextravagal effects of digitalis glycosides on theconducting system,8'0 the therapeutic successof atropine in these obviously toxic patientsunderscores its potential role in the manage-ment of digitalis-induced SA or A-V block. Acase similar to our case 1 has been describedby Surawicz and Mortelmans, in whichatropine abolished depression of SA nodeactivity (or exit block) in a healthy 17-year-old woman following suicidal ingestion ofdigitoxin."1 It may be that the generallyunfavorable experience with atropine in digi-talis-induced A-V block reported by someauthors'2 is relevant chiefly to situations inwhich digitalis has been administered chron-ically to patients with diseased hearts; thecases reported here differ both in the absenceof preexisting heart disease and in the acutenature of the toxic insult. The efficacy ofatropine in reversing digitalis-induced A-Vblock has also been noted by Miller.13The third patient with no prior history of

cardiac disease succumbed with refractoryhyperkalemia and high grade A-V blockdespite the most vigorous and sophisticatedsupportive efforts. This patient had a serum

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SMITH, WILLERSON

digoxin level of 42 ng/ml 4 hr after theingestion, which is the highest level we haveobserved in over 6000 determinations coveringa broad spectrum of clinical circumstances.The occurrence of refractory hyperkalemia inthis case is of interest, and suggests thatgeneralized inhibition of the sodium-po-tassium activated adenosine triphosphatase(ATPase) of the cell membrane may haveoccurred with this massive dose of cardiacglycoside, resulting in impairment of theability of cells to maintain the normally highratio of intracellular to extracellular potassiumconcentration. 415 Consistent with this hypo-thesis are the observations of Gaultier et al.,5who found an elevated mean serum potassiumlevel following acute ingestion of largeamounts of cardiac glycosides compared withnondigitalized control subjects; cases with afatal outcome, in turn, had a higher meanlevel than that of those patients who survived.Thus, despite its usefulness in many cases ofdigitalis intoxication characterized by ectopicimpulse formation, supplemental potassiummay increase A-V block and should not beused as a matter of routine without dueconsideration of the type of rhythm distur-bance, serum potassium concentration, andrenal function.'0The possibility that propoxyphene intoxica-

tion played a role in this patient's demisecannot be excluded. Transient QRS wideninghas been observed in association with seizures,apnea, and cyanosis in a reported case ofsevere propoxyphene intoxication, but therewas no evidence of A-V block or electrolytedisturbance.16 It seems reasonable to presumethat the primary clinical problems in this casewere directly related to digoxin intoxication.The remaining two patients exhibited fre-

quent ventricular premature beats with epi-sodic ventricular tachycardia or ventricularfibrillation during the initial 24 hr afteringesting the digoxin. In both instances A-Vblock appeared after the ventricular excitabil-ity had diminished under the influence ofantiarrhythmic drugs. Both of the latter twopatients had coronary artery disease withprevious myocardial infaretions. This experi-

ence is consistent with previous observationsthat the response of the normal human heartto digitalis excess tends to be development ofA-V conduction disturbances, while the dis-eased heart frequently responds with ectopicimpulse formation, particularly from ventricu-lar foci.1' 2, 17, 18An interesting analogy to these observations

in normal hearts may be found in pediatricclinical experience, where P-R interval pro-longation constitutes a frequent sign ofimpending digitalis excess and the suddenemergence of ectopic ventricular arrhythmiasas a manifestation of digitalis intoxication isuncommon.1'9 20 One may speculate that theabsence of coronary artery disease withattendant areas of focal ischemia may be animportant factor. The converse of this situa-tion may be reflected in the increasedincidence of coronary artery disease amongadult patients who exhibit digitalis intoxica-tion at relatively low serum concentrations ofdigoxin or digitoxin.21 22The apparent serum half-times for digoxin

clearance exhibited by these patients are ofinterest. The mean serum half-time for orallyadministered tritiated digoxin following tissueuptake and distribution in subjects withnormal renal function is about 31 hr.23 Thisplateau is reached within about 6 hr after oraldoses of digoxin.23 24 Although the data fromcases 1, 2, 3, and 4 allow only approximationsof serum half-times, the range of values fromabout 6 to 22 hr for samples drawn 5 or morehr after the ingestion represents a departurefrom the expected mean. The more detaileddata from case 5 (see fig. 4) indicate that onlyafter 48 hr, when the serum level has fallen tothe usual range encountered in patients ontherapeutic doses of digoxin, does the serumhalf-time reach the expected value of 32 hr.One explanation of these results lies in thepossibility that gastrointestinal absorption ofthese larger doses was slowed, and that tissueuptake and distribution was occurring laterthan usual. The relatively high level at 13 hrcompared with that at 1 hr in case 1 iscompatible with a prolonged phase of gastro-intestinal absorption. Hence a relatively late

Circulation, Voluzme XLIV. July 1971

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DIGOXIN INGESTION

serum peak with continuing tissue uptake mayhave combined with renal clearance to shortenthe serum half-times in some cases. However,since gut absorption of digoxin appears to be apassive process without evidence of saturationkinetics,25 this mechanism must remain conjec-tural. Alternatively, it may be that the half-time for tissue uptake and distribution isprolonged with massive doses, independent ofthe rate of gastrointestinal absorption. Hereagain, the combined effects of tissue uptakeand renal excretion would be operative duringthe period when renal excretion alone domi-nates the clearance from the serum of usualdoses. Finally, it may be that the relationshipbetween tissue and serum levels is alteredwith massive ingestions in favor of higherserum: tissue ratios, resulting in a relativelygreater proportion of the total body burden ofdrug being presented to the glomerulus perunit time for filtration and excretion.The clinical experience reported here indi-

cates that accidental or suicidal digoxinintoxication can be successfully managed inmost cases by appropriate use of antiarrhyth-mic and vagolytic drugs combined, whennecessary, with temporary pervenous pacingtechniques. The death of a previously healthyyoung woman following massive digoxiningestion, however, underscores the need formore effective therapeutic modalities in suchinstances.

AcknowledgmentThe authors are grateful to Doctors Bernard Lown,

Thomas J. Ryan, and James J. Sidd for theopportunity to include patients under their care in thisstudy.

References1. BERGY GG, FERGUS EB, BRUCE RA: Acute

massive digitoxin poisoning; report of a caseand review of the literature. Ann Intern Med46: 964, 1957

2. FOWLER RS, RATHI L, KEITH JD: Accidentaldigitalis intoxication in children. J Pediat 64:188, 1964

3. BUCHANAN J: Self-poisoning with digitalis glyco-sides. Brit Med J 3: 661, 1967

4. McNAMARA DC, BREWER EJ JR, FERRY CD:Accidental poisoning of children with digitalis.New Eng J Med 271: 1106, 1964


5. GAULTIER M, FOURNIER E, E1rHyMIou M-L,FREJAVILLE J-P, JOUANNOT P, DENTAN M:Intoxication digitalique aigue. Bull Soc MedHop Paris 119: 247, 1968

6. SMITH TW, BUTLER VP JR, HABER E: De-termination of therapeutic and toxic serumdigoxin concentrations by radioimmunoassay.New Eng J Med 281: 1212, 1969

7. SMITH TW, HABER E: Digoxin intoxication: therelationship of clinical presentation to serumdigoxin concentration. J Clin Invest 49: 2377,1970

8. MOE GK, FARAH AE: Digitalis and allied cardiacglycosides. In The Pharmacological Basis ofTherapeutics, edited by LS Goodman, ACilman, Ed 3. New York, Macmillan Co., 1965,p 673

9. FiscH C, GREENSPAN K, KNOEBEL S, FEIGEN-BAuM H: Effect of digitalis on conduction ofthe heart. Progr Cardiovasc Dis 6: 343, 1964

10. FISCH C, KNOEBEL SB: Recognition and therapyof digitalis toxicity. Progr Cardiovasc Dis 13:71, 1970

11. SURAWICz B, MORTELMANS S: Factors affectingindividual tolerance to digitalis. In Digitalis,edited by B Surawicz, C Fisch. New York,Grune & Stratton, Inc., 1969, p 127

12. FRIEDBERG CK, DONOso E: Arrhythmias andconduction disturbances due to digitalis. ProgrCardiovasc Dis 2: 408, 1960

13. MILLER PH: Efficacy of atropine in thetreatment of digitalis induced AV block. DisChest 56: 229, 1969

14. SCHATZMANN HJ: Herzglykoside als Hemmstoffefiur den aktiven Kalium-und Natrium-transportdurch die Erythro-cytenmembran. Helv PhysiolPharmacol Acta 11: 346, 1953

15. PAGE E: The actions of cardiac glycosides onheart muscle cells. Circulation 30: 237,1964

16. QuREsm EH: Propoxyphene hydrochloride poi-soning. JAMA 188: 170, 1964

17. PICK A: Digitalis and the electrocardiogram.Circulation 15: 603, 1957

18. PICK A, IGARASHI M: Mechanism, differentialdiagnosis, and clinical significance of digitalis-induced arrhythmias. In Digitalis, edited by BSurawicz, C Fisch. New York, Grune &Stratton, Inc., 1969, p 148

19. NADAS AS: Padiatric Cardiology, Ed 2. Philadel-phia, W. B. Saunders Co., 1963, p 90

20. NEILL CA: The use of digitalis in infants andchildren. Progr Cardiovasc Dis 7: 399, 1965

21. SMITH TW: Radioimmunoassay for serum digi-toxin concentration: methodology and clinicalexperience. J Pharmacol Exp Ther 175: 352,1970

22. BELLER GA, SMITH TW, ABELMANN WH, HABERE, HOOD WB JR: Digitalis intoxication: a

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prospective clinical study with serum levelcorrelations. New Eng J Med 284: 989, 1971

23. DOHERTY JE: The clinical pharmacology ofdigitalis glycosides: a review. Amer J Med Sci255: 382, 1968

24. WHITE RJ, CHAMBERLAIN DA, HOWARD MR,

SMITH TW: Plasma concentrations of digoxinafter oral administration in the fasting andpostprandial state. Brit Med J 1: 380, 1971

25. CALDWELL JH, MARTIN JF, DUTITA S, GREEN-BERGER NJ: Intestinal absorption of digoxin-3Hin the rat. Amer J Physiol 217: 1747, 1969

Correction

Baron MG: Circulation 43: 768, 1971. Figures7A and 7B were incorrectly labeled.What is now figure 7A should be figure 7B,

and what is now figure 7B should be figure 7A.


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THOMAS W. SMITH and JAMES T. WILLERSONDigoxin Level Correlations

Suicidal and Accidental Digoxin Ingestion: Report of Five Cases with Serum

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1971 American Heart Association, Inc. All rights reserved.

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Suicidal and Accidental Digoxin Ingestion - Circulationcirc.ahajournals.org/content/circulationaha/44/1/29.full.pdf · Suicidal and Accidental Digoxin Ingestion Report of Five Cases