Meth Case Study

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Methamphetamine Case Study

By Ruth “Missy” Jensen, MSN, FNP

INTRODUCTION

Methamphetamine use is a growing drug-abuse problem in the United States with the

National Institute for Drug Abuse reporting that nearly 12 million Americans have triedmethamphetamine. Methamphetamine is a very addictive stimulant drug that activates

certain systems in the brain. It is chemically related to amphetamine but, at comparable

doses, the effects of methamphetamine are much more potent, longer lasting, and moreharmful to the cardiovascular and central nervous systems.

Methamphetamine increases the release of very high levels of the neurotransmitterdopamine, which stimulates brain cells, enhancing mood and body movement. Taking even

small amounts of methamphetamine can result in increased wakefulness, increased physical

activity, decreased appetite, increased respiration, rapid heart rate, irregular heartbeat,

increased blood pressure, and hyperthermia. Other effects of methamphetamine abuse mayinclude irritability, anxiety, insomnia, confusion, tremors, convulsions, and cardiovascular

collapse and death. Long-term effects may include paranoia, aggressiveness, extreme

anorexia, memory loss, visual and auditory hallucinations, delusions, and severe dental problems.

Though the full effect of methamphetamine on the cardiovascular system has not been

thoroughly described in the literature, several case reports and small-scale studies have been published.

CASE PRESENTATION

43 y/o female patient presents to Urgent Care complaining of three-to-four week

history of shortness of breath, fatigue, “restlessness” at night and chest “pressure”

that has been unrelenting for the past 12 hours.

PMH

Denies any previous medical history, is on no regular medications

SOCIAL HISTORY

Divorced, had 2 grown children locally. Works for the county as an EMS dispatcher.

Smokes 1ppd (25-30 pack-year). Denies alcohol. Uses oral methamphetamine daily

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(usually twice a day) for the past 1 ½ years. Admits to cocaine use “once or twice”several years ago.

FAMILY HISTORY

Father has history of alcohol abuse and questionably HTN, otherwise negative.

CARDIOVASCULAR RISK

Smoker

Hypertensive (on presentation—no history)

PHYSICAL EXAM

Anxious/nervous appearing, obviously short of breath VS: BP 172/120; HR 120; RR 24; Temp 99.9; O2 Sat 97%;? WT

HEENT: PEERL, Conjunctiva Pink/Moist; Lips dry/cracked

NECK: JVP ~ 10 cm with clear hepato-jugular reflux. No Bruit

LUNGS: Good inspiratory effort with bi-basilar “crackles”

CV: RRR, HR 118, no S3 described, no murmur

ABD: no hepatomegaly; no fluid wave

EXT: 1+ pre-tibial edema

SKIN: good turgor

DIAGNOSTICS & LABS

Na 139, K+ 4.1, CL 107, Glucose 105, BUN 10, CR 1.0 TSH 1.05

BNP 1782

Troponin < 0.2, CKMB 1.5

UDS (drugs of abuse screen): positive for amphetamine and benzodiazepines

EKG: Sinus Tachycardia, normal axis/intervals, occasional PVCs

ECHO: Normal Left Ventricle size, but severely decreased LV systolic functionwith EF 15-20%

HOSPITAL COURSE:

Admitted from urgent care to the cardiovascular care unit for evaluation. Cardiacenzymes were cycled, and she ruled-out for an acute coronary syndrome.

Echocardiogram was done on Day 1. She underwent diuresis with furosemide

infusion and was asymptomatic by end of Day 2. ACE-Inhibitor and Beta-Blockertherapies were started using lisinopril and carvedilol.

Day 3 patient was clinically opti-volemic. Heart Failure Management Program

evaluated patient. Aldosterone Antagonist therapy started with spironolactone. HF



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education was started, and included discussion of methamphetamine as cause of hercardiomyopathy. HF nutrition counseling provided by registered dietician.

Psychiatric/Addictions care also evaluated patient. She refused

Inpatient and outpatient addictions treatment.

Day 4 discharge to home in care of her son. To follow up in the Heart Failure Clinicin four days.

OP HF CLINIC FOLLOW UP-1

Patient seen four days post-discharge feeling much better and compliant withmedications. No methamphetamine and no cigarettes since hospital admission.

Counseling by HF NP, Clinical Pharmacist and Registered Dietician.

Medications: carvedilol, lisinopril, furosemide, spironolactone, and lexapro. Carvedilol up-titrated to 6.25 mg BID

Chemistry panel: NA 137, K+ 4.1, BUN 18, CR 1.1

BNP: 594

Non-invasive impedance cardiography (BioZ): Increased vascular resistance (2044),

reduced cardiac output (3.3), reduced stroke index (25).

Patient again refused outpatient addictions counseling, agrees to weekly follow-upwith HF clinic.

SUBSEQUENT HFC FOLLOW UP

Patient seen weekly for next 6 weeks.

Carvedilol titrated to 25 mg BID Furosemide decreased to 40 mg daily over time

Remained abstinent from methamphetamine (UDS negative), but started smoking

again after about 8 weeks.

Three months after HFC therapy was initiated, the ECHO was repeated:o LV systolic function NORMAL. EF 72%

Two months after the echocardiogram, patient failed follow up with HFC.

She did return for one visit at which she admitted that she used methamphetamine

one time in the previous week after the death of her grandmother. She again refusedaddictions treatment/counseling.

She has not returned to HFC since that visit.

Multiple attempts have been made to locate/contact patient via telephone and mail.

She has moved and all of her emergency contacts claim to not know her

whereabouts.

DICUSSION

Methamphetamine (and cocaine) use should be considered any time a young person



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presents with new-onset heart failure associated with significant hypertension.

Refusal to participate in clinical addictions recovery and counseling programs is

common in drug-addicted persons.

Several studies have documented adverse effects of beta-blockade in patients with

ongoing cocaine or amphetamine use. The hazard lies in the potential for deadlyventricular arrhythmias with unopposed beta-blockade concomitantly with

amphetamine agents. Though no large-scale, randomized studies exist, the use of an

alpha & beta-blocking agent (such as carvedilol) is widely felt to reduce the potential for adverse cardiac events in this population.

Methamphetamine-induced cardiomyopathy can very often be successfully treated

with significant improvement in systolic function with a combination of abstinence

from the drug and a medication regimen of beta-blocker, ACE-inhibitor, andaldosterone antagonist.

However the disease of addiction cannot be ignored. The potential for relapse is

great. As addictions research has shown, drug-addicted persons are at risk of

stopping therapeutic medication regimens, relapse, and poor follow-up habits.



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REFERENCES

1. National Survey on Drug Use and Health - SAMHSA web site.2. National Institute on Drug Abuse. Epidemiologic Trends in Drug Abuse: Advance

Report, Community Epidemiology Work Group, January 2006. NIH Pub.

No. 06-5878, Bethesda, MD: NIH, DHHS, 2006.3. Petry NM, Peirce JM, Stitzer ML, Blaine J, Roll JM, Cohen A. Obert J, Killeen T,

Saladin ME, Cowell M, Kirby KC, Sterling R, Royer-Malvestuto C,

Hamilton J, Booth RE, Macdonald M, Liebert M, Rader L, Burns R, DiMariaJ, Copersino M, Stabile PQ, Kolodner K, Li R. Effect of prize-based

incentives on outcomes in stimulant abusers in outpatient psychosocial

treatment programs: a national drug abuse treatment clinical trials network

study. Arch Gen Psychiatry 62(10):1148–1156, 2005.4. Call T, Hartneck J, Dickenson W, Hartman C, Bartel A. Acute cardiomyopathy

secondary to intravenous methamphetamine abuse. Ann Intern Med. 1982;

97: 559-560.5. Smith H, Roche A, Jagusch M, Herdson, P. Cardiomyopathy associated with

amphetamine administration. An Heart J. 1976; 91:792-797.

6. Nestor T, Tamamoto W, Kam T, Schultz T. Crystal methamphetamine-induced pulmonary edema: a case report. Hawaii Med J. 1989; 48:457-460.

7. Hong R, Matsuyama E, Nur K. Cardiomyopathy associated with the smoking of

crystal methamphetamine. JAMA. 1991; 265: 1152-54.

8. Islam MN, Kuroki H, Hongcheng B, Ogura Y, Kawaguchi N, Onishi S, WakasugiC. Cardiac lesions and their reversibility after long term administration of

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Meth Case Study