0% found this document useful (0 votes)
96 views45 pages

Medical Complications of Alcohol Use: Moderator: DR Spoorthy Presenter: DR Neethu

This document discusses the various medical complications that can arise from alcohol use in multiple body systems. It covers effects in the nervous system like intoxication, withdrawal seizures, and nutritional deficiencies. Gastrointestinal complications mentioned include gastritis, pancreatitis, and liver disease progression to cirrhosis. Cardiovascular risks discussed are increased risk of heart attack and cardiomyopathy. Other systems affected include the hematopoietic and genitourinary systems, as well as increased risk of certain cancers.

Uploaded by

Sensible
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
96 views45 pages

Medical Complications of Alcohol Use: Moderator: DR Spoorthy Presenter: DR Neethu

This document discusses the various medical complications that can arise from alcohol use in multiple body systems. It covers effects in the nervous system like intoxication, withdrawal seizures, and nutritional deficiencies. Gastrointestinal complications mentioned include gastritis, pancreatitis, and liver disease progression to cirrhosis. Cardiovascular risks discussed are increased risk of heart attack and cardiomyopathy. Other systems affected include the hematopoietic and genitourinary systems, as well as increased risk of certain cancers.

Uploaded by

Sensible
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
You are on page 1/ 45

MEDICAL COMPLICATIONS

OF ALCOHOL USE
MODERATOR: DR SPOORTHY
PRESENTER: DR NEETHU
SCHEME

 INTRODUCTION

ADVERSE EFFECTS IN
 NERVOUS SYSTEM
 GASTROINTESTINAL SYSTEM
 CARDIOVASCULAR SYSTEM
 HAEMATOPOETIC SYSTEM
 GENITOURINARY SYSTEM
 CANCERS
 TERATOGENECITY
 OTHERS
 CONCLUSION
INTRODUCTION
 Alcohol is the most common substance abuse.

 Alcohol is a psychoactive drug that depresses the central nervous system.

 Acts on GABA A receptors

 Alcohol cause both acute and chronic changes in almost all neurochemical systems.

 Several preexisting psychiatric diagnosis including antisocial personality , bipolar and


schizophrenic disorder includes the risk of later alcohol use disorder.

 most affected systems: liver , respiratory and cardiovascular


NERVOUS SYSTEM
 ACUTE INTOXICATION
 ALCOHOLIC BLACK OUT
 ALCOHOLIC DEMENTIA
 DELIRIUM TREMENS
 WITHDRAWAL SEIZURES
 WERNICKE’S ENCEPHALOPATHY
 KORSAKOFF’S PSYCHOSIS
 PERIPHERAL NEUROPATHY
 STROKE
 CEREBELLAR DEGENERATION
 AMBLYOPIA
 CENTRAL PONTINE MYELINOSIS
 MARCHIFAVA - BIGNAMI DISEASE
 Alcohol intoxication
acute intoxication
pathological intoxication
blackouts
 Alcohol withdrawal syndromes
tremors,
hallucinosis ,
seizures ,
delirium tremens.
 Nutritional defects:
Wernicke’s encephalopathy,
Korsakoff’s syndrome,
peripheral neuropathy
cerebellar degeneration,
amblyopia.
ACUTE ALCOHOL INTOXICATION
 A reversible syndrome caused by recent ingestion of alcohol
 Effects of alcohol are sensitive to dose.
 Early effects produce elation, excitement
Physiological signs of intoxication :
slurred speech
dizziness
incoordination
unsteady gait
nystagmus
impairment in attention / memory
BLOOD LEVEL IMPAIRMENT
20-30 mg/dl Slowed motor performance &
decreased thinking ability.

30-80 mg/dl Increases in motor & cognitive


problems
80-200 mg/dl Increase in incoordination &
judgement errors, mood
lability,deterioration in cognition

200-300 mg/dl Nystagmus, marked slurring of


speech and alcoholic blackouts.

>300 mg/dl impaired vital signs & possible


death
PATHOLOGICAL INTOXICATION

 Abrupt irrational combative behaviour , after taking small amounts of


Alcohol that would have minimal behavioural effects on most persons.
 Its is called as acute alcohol paranoid state/idiosyncratic
intoxication/manie a potu
ALCOHOLIC BLACKOUTS

 Dense amnesia for significant events that have occurred during a drinking
episode.
 Alcohol interferes with the transfer of information from short term to long
term storage
WITHDRAWAL SEIZURES

 Alcohol can precipitate seizures in a person suffering from epilepsy .


 Withdrawal seizures : 12-48hr of the termination of long continued bout.
 Usually generalized tonic clonic seizures.
 EEG-abnormal at time of seizures.
 High risk of progression to delirium tremens.
DELIRIUM TREMENS
 Delirium tremens is the most severe form alcohol withdrawal .
 MEDICAL EMERGENCY
 Hospitalise
 Full blown DT: profound confusion, vivid hallucinations, marked tremor,
agitation, sleeplessness and autonomic disturbances.
 Presence of hallucination with two of the following: confusion and
disorientation, tremulousness, increased PMA, fearfulness and signs of
autonomic disturbance.
Risk factors

 Daily heavy and prolonged ethanol consumption


 Severe withdrawal symptoms at presentation
 Intense craving for alcohol
 Older age
 Past history of DT
 Withdrawal seizures
 Presence of acute medical comorbidity, especially infections
etiology

 A primary disorder of the reticular formation is strongly suggested by the


clinical components of profound inattention coupled with alertness,
overactivity and insomnia.

 Cerebral blood flow studies :


increased CNS excitability during the course of delirium.

 Withdrawal of alcohol
treatment

 Best treatment is prevention.


 In terms of slow bolus dose of IV diazepam 5-10mg or IV lorazepam 2-4 mg
 CIWA-Ar >20: give bolus  monitor every 10-20 min  repeat every time till
CIWA-Ar <10
 CIWA-Ar <10: monitor every 1-2 hour for 12 hours
 Aim is to sedate the patient
 Antipsychotic medication should be avoided
 Supportive care:
Correct dehydration
Environmental reorientation measures.
WERNICKE’S ENCEPHALOPATHY

 It is an acute complication due to severe thiamine deficiency.

 Characterised by nystagmus, abducens and conjugate gaze palsies,


ataxia of gait, and global confusional state.

 Role of thiamine:
Thiamine is phosphorylated to TPP, which acts as a coenzyme.
INVESTIGATIONS

 EEG: asynchronous slow waves and often also causes bisynchronous slow
waves.

 CSF: mild elevation of protein

 CT: symmetrical areas of decreased attenuation in the region of the


thalamus

 MRI: atrophy of the mamillary bodies


hyperintensities surrounding the third ventricle
TREATMENT

 Acute medical emergency.


 Pabrinex is usually employed intravenously in place of thiamine alone.
 Inj.Pabrinex(thiamine hydrochloride250 mg, nicotinamide 160 mg, ribofl
avine 4 mg,
pyridoxine hydrochloride 50 mg and ascorbic acid 500 mg) twice daily for
atleast 5 days.

 Oral vitamin supplements are usually continued for


several weeks after the acute illness has resolved .(3 months)
 If delayed nicotinic acid deficiency encephalopahy must be considered.
KORSAKOFF’S SYNDROME

 Korsakoff’s syndrome is an amnestic syndrome caused by thiamine


deficiency.

 Clinical features:
anterograde and retrograde amnesia., confabulation.

 Neuroimaging findings:

 CT: cortical shrinkage and ventricular dilatation.
atrophy in frontal sulcal and perisylvian areas
Contd..

 MRI: loss of grey matter in the medial temporal and orbitofrontal cortex

 FDG-PET : hypometabolism present in numerous cortical areas ,


involvement of the thalamus and basal ganglia

 Treatment:
thiamine replacement
iv thiamine 500mg,2-3 times/day for 3-5 days.
oral T.thiamine 100mg/day. Amnesia, apathy and may not improve
ALCOHOLIC COGNITIVE IMPAIRMENT

 Long term cognitive problem that can develop in course of AUD-alcohol


induced persisting dementia

 Global decrease in intellectual function, cognitive abilities and memory,


psychomotor speed, visuospatial competence and new learning ability.

 CT: enlarged ventricles and shrinkage of cerebral sulci, widening of gyri


and fissures.

 MRI: reduction in grey matter in medial temporal, superior frontal, and


parietal regions, sub cortical grey matter.
CEREBELLAR DEGENERATION

 Ataxia most common feature. Hands less involved. Nystagmus , dysarthria less
common.
 May be asymptomatic
 CT/ MRI: cerebellar cortical atrophy
 FDG-PET: hypometabolism in superior cerebellar vermis

STROKE
 Increase in LDL (type hyper lipidemia)
 Increase in cholesterol, triglycerides
 Increased BP
MARCHIFAVA– BIGNAMI DISEASE
 Cause: demyelination of corpus callosum.

 Clinical features:
ataxia, dysarthria ,epilepsy ,
severe impairment of consciousness.
• slowly progressive form :dementia and spastic paralysis of limbs.

 Investigation:
 CT & MRI: characteristic finding of demyelination in corpus callosum
CENTRAL PONTINE MYELINOSIS

 acute and often fatal complication of alcoholism.

 Clinical features:
obtundation ,bulbar palsy, quadriplegia &
loss of pain sensation in limbs and trunk.
Vomiting ,confusion ,disordered eye movements.

 Location: lesion at center of basis pontis


 MRI: focus of demyelination
PERIPHERAL NEUROPATHY

 Cause: deficiency of thiamine, pyridoxine and pantothenic acid.

 Clinical features: sensory ataxia, foot drop, cutaneous sensory loss.

 Treatment: vitamin supplementation


AMBLYOPIA

 retrobulbar neuritis.
 Clinical features:
dimness of central vision ,especially for red & green.
 Acute blindness-methyl alcohol consumption
GASTROINTESTINAL SYMPTOMS

 ACUTE HAEMORRHAGIC GASTRITIS AND ESOPHAGITIS (acute)


 MALLORY- WEISS TEARS (acute)
 ACUTE PANCREATITIS
 CHRONIC PANCREATITIS
 STEATOHEPATITIS TO CIRRHOSIS TO HEPATIC ENCAPHALOPATHY (chronic)
 Most common cause of hemorrhagic gastritis

 Violent vomiting leads to longitudinal tear in mucosa in gastroesophageal


junction.

 Acute pancreatitis: abdominal pain radiating to back, nausea and


vomiting , anorexia . H/o binging on alcohol

 Chronic pancreatitis: most common cause of chronic pancreatitis in adults.


May occur After repeated bouts of acute pancreatitis. Pseudocyst may be
present, may lead to diabetes.
Contd…

 Steatohepatitis: AST > ALT

decreased beta
impaired increased lactate fat deposition
oxidation of fatty
gluconeogenesis production inside hepatocytes
acid

 Alcoholic hepatitis: immunologically mediated, interleukins are implicated.


Severe alcoholic hepatitis treated with prednisone or prednisolone or
pentoxyphylline.
HEPATIC ENCEPHALOPATHY

 Etiology: brain edema, gut derived


neurotoxins and ammonia

 Impaired consciousness, personality


changes, sleep disturbances,
asterixis.

 Treatment: taking care of


precipitating factors: like GI bleed,
SBP, infections etc.
 lactulose, metronidazole,
neomycin, rifaximin, zinc
supplementation.
CARDIOVASCULAR SYSTEM

 MYOCARDIAL INFARCTION: increased risk of cardio vascular diseases due


to impaired lipid profile.

 CARDIOMYOPATHY: direct effect of alcohol on myocardium. Dilatation of


all the 4 chambers of heart leading to pump failure.

 PAROXYSMAL TACHYCARDIA: atrial or ventricular arrhythmias with no


apparent evidence of heart disease. Holiday heart syndrome
HAEMATOPOIETIC SYSTEM

 INCREASED MCV: folic acid deficiency, cholesterol deposition in rbc


membrane, sideroblastic changes in marrow

 DECREASED IMMUNE FUNCTIONS: decreased production of WBCs,


decreased granulocyte mobility and adherence. Decreased delayed
hypersensitivity reaction.

 THROMBOCYTOPENIA: idiopathic, hypersplenism


GENITOURINARY SYSTEM

 DECREASED ERECTILE CAPACITY : increased sexual drive, but decreased


erectile capacity

 TESITICULAR ATROPHY :even in absence of ALD, irreversible shrinkage of


testis, with shrinkage of seminiferous tubules, decreased ejaculate volume
and low sperm count.

 INFERTILITY IN WOMEN: decreased ovarian size and absence of corpora


lutea

 INCREASED RISK OF SPONTANEOUS ABORTIONS


CANCERS

 INCREASED RISK OF BREAST CANCER


 ESOPHAGEAL CANCER
 RECTAL CANCER
 STOMACH CANCER
 COLON CANCER
 LIVER CANCER
 CANCERS OF HEAD AND NECK
 LUNG CANCER

 Cancer promoting action of alcohol and acetaldehyde impairing immune


homeostasis
FETAL ALCOHOL SYNDROME
 INCIDENCE: 0.2-1.5 cases per 1000 live
birth (in some studies)
 5% of children born to heavy drinking
mother.
 LOW IQ
 SMALL HEAD
 LBW WITH FACIAL ANOMALIES
 ASDs or VSDs

FETAL ALCOHOL SPECTRUM


DISORDER:
 MODEST COGNITIVE DEFICITS
 HYPERACTIVITE BEHAVIOR
 LOW IQ
OTHERS

 ALCOHOLIC MYOPATHY: direct effect of alcohol. Might not remit fully on


abstinence.
 HORMONAL CHANGES: increased cortisol levels, decreased T3 and T4.
 EFFECTS ON SKELETAL SYSTEM: low bone mineral density
 CATARACTS
 BERIBERI: thiamine deficiency
 HYPOGLYCEMIA
CONCLUSION

 Alcohol - one of the most common substance of abuse


 Complications can occur due to acute binge intake or chronic alcohol
intake and due to withdrawal.
 Affects various systems of the body
REFERENCES

 Kaplan & sadocks comprehensive textbook of psychiatry.10th edition.


 Lishman’s organic psychiatry.
 Harrison’s principles of internal medicine 19th edition.
THANK YOU

You might also like