Family Medicine Revision course 26 TH -30 TH JANUARY 2015 1 DR. V.M ALABI. FMCGP, FWACP.

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MANAGEMENT OF CHOLERA Family Medicine Revision course 26 TH -30 TH JANUARY 2015 1 DR. V.M ALABI. FMCGP, FWACP

Transcript of Family Medicine Revision course 26 TH -30 TH JANUARY 2015 1 DR. V.M ALABI. FMCGP, FWACP.

Page 1: Family Medicine Revision course 26 TH -30 TH JANUARY 2015 1 DR. V.M ALABI. FMCGP, FWACP.

1

MANAGEMENT OF

CHOLERAFamily Medicine Revision course26TH -30TH JANUARY 2015

DR. V.M ALABI.

FMCGP, FWACP

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Cholera is : An acute bacterial diarrhoeal infection Caused by gram negative bacterium Vibrio cholerae Usually ingested from food or water contaminated by

faecal material Affects children and adults Affects only the small intestine The enterotoxin secreted in the epithelium of the

intestine causes increased activity of adenylate cyclase, resulting in

↑ secretion of water and salts into the lumen of the gut. Leads to diarrhoea and loss of electrolytes.

DEFINITION/INTRODUCTION

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Cholera originated from the Ganges delta in the India sub-continent

Spread across the world in the 19th century, along trade routes

Epidemics have occurred in Russia, Western Europe and North America.

Pandemics have occurred in Asia, Africa and Latin America with millions of death.

Seven pandemics have occurred since 1817. Most resent outbreaks occurred in Haiti (2010) and

Nigeria(2011) In 2011 ;58 countries were affected, 589,854

cases;7816 deaths.

HISTORY

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Cholera: Water borne disease Transmitted via contaminated food or water Found in slums- a disease of poverty Occurs also in travellers to endemic regions

Associated with seasonal peaks- warm climate. Between 1995 and 2005, about half a million people

were estimated affected in war torn areas – DRC of Congo and Rwanda.

Large outbreaks have occurred in South-East Asia In 2010, more than 120,000 cases with a case-

fatality rate of 2.1% was reported in HaIti.

EPIDEMIOLOGY

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Children under five are more affected in endemic areas

Adult are more affected in less endemic regions. Clinical presentation is affected by level of

nutrition, background immunity and bacterial load

cholera remains a public health problem in developing countries

Attributed to poor /inadequate water treatment, poor personal hygiene and poor sanitary facilities.

EPIDEMIOLOGY

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First outbreak reported in 1971 22931 cases and 2945 death were reported; 12.8%

case fatality rate(CFR) Intermittent outbreaks have been reported between

1972 and 1990 Jan – Dec 2010 a severe outbreak started from the

northern part and spread to other part. 41787 cases, 1716 deaths(CFR 4.1%)

222LGAs were affected in 18 states. Most affected states were Brono, Bauchi and Katsina 2011, between April and October , 22454 cases, 715

deaths (CFR 3.2%) was reported in 195 LGAs.

CHOLERA EPIDEMIOLOGY IN NIGERIA

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• Vibrio cholerae is- a non spore forming, gram negative ,curved rod shaped bacterium.

• Thrives in brackish water which serves as reservoir for human infection.

• Attaches to tiny planktonic crustaceans. • It feeds on the chitin(sugar polymer found on the

shell of the crustaceans) and . . Causes infection when such sea foods are eaten raw or undercooked.

Several serotypes based on their antigenic characteristics are known.

THE ORGANISM

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THE ORGANISM VIBRIO CHOLERA

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Two main biotypes are known i- Classical ii- El Tor Both have two serotypes i Inaba ii Ogawa no major clinical difference is found between the two serotypes

or biotypes. Infection is caused by toxigenic strains of serotype O1 and O139 Most outbreaks/pandemics are caused by serotype O1 O139 is restricted to SE Asia where it was first identified in

Bangladesh in 1992. Non-O1 and non O139 are known to cause diarrhoeal diseases

similar to classical cholera but not outbreaks.

AETIOLOGY

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When ingested in food or water : The organism attaches to the epithelial surface to the small

intestines an multiplies fast Produces potent toxin- a protein with five binding units,

which attaches to some receptors on the intestinal wall. Enzyme adenylate cyclase is activated and breaks down

ADP(adenosine diphosphate) to cyclic adenosine monophophste(cAMP).

Interferes with normal fluid and salts movement, ↑ chloride secretion, ↓ NaCl reabsortion.

Results in massive volume of diarrhoea Watery stools loaded with the organism result Can result in outbreaks if stool contaminates water

sources.

PATHOPHYSIOLOGY

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Poor sanitary conditions Displaced population with overcrowding with inadequate

basic infrastructures(water and sanitation); found in refuge camps, war torn areas, flood natural disaster areas.

Slums Poor or inadequate water treatment Poor personal hygiene Ingestion of raw or undercooked sea foods ↓ or lack of stomach acid(hypochlohydria) e.g children Adults on antacids who lack acid enviroment in their

stomach People with O type blood group ( ? Reason) Household exposure

RISK FACTORS

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Most people( 75%) infected are asymptomatic or have a mild disease.

Asymptomatic person may continue to excrete the organism in stool for 7-14 days

About 7-10% develop symptoms Incubation period is few hour after exposure to 5 days Passage of profuse, pale and milky stools (rice water)› 1 litre/hour Or › 20mL/kg in a four hour observation period. Nausea and vomiting( common in children) Fever* Abdominal pain * Mild- moderate dehydration Severe dehydration Dehydration could set in within hours of onset

SYMPTOMS

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Mild dehydration – fluid loss is <10% of body weight

Severe dehydration –fluid loss ≥ 10% of body wt.

About 80% of people affected develop mild to moderate symptoms

About 20% develop severe dehydration

SYMPTOMS CONT’D

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Mild – moderate dehydration: ↑thirst Dry mucous membrane/ tongue ↓skin turgor Irritability Restlessness ↓anterior fontanelle in infants ↓urine output Sunken eyes

DEHYDRATION

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Severe dehydration leads to circulatory collapse Hypotension(SBP< 80mmHg) Weak /Thready pulse Very dry mucous membrane/tongue Sunken eyes Oliguria/anuria Muscle cramps Poor skin turgor Lethargy Unconsciousness Hypoglycaemia especially in children- seizures and

coma

SEVERE DEHYDRATION

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Hypoglycaemia Hypokalaemia → paralytic ileus;arrhythmias Muscle cramps Shock – circulatory collapse Acute renal failure Death

COMPLICATIONS

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History - travel - Social hx (contact,family -food ingested ( sea foods?) - drug Physical examination Lab tests- FBC -Electrolytes - urea and creatinine - rapid cholera dipstick test of the stool( crystal VC

dipstick)

DIAGNOSIS

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Other causes of infectious diarrhoea May be difficult to differentiate in early

stages Shigella - bloody stool Enterohaemorrhagic E coli - bloody stool Amoebic diarrhoea – not large

volume,bloody Giardiasis - eggs,live parasites Food poisoning In all these, stool culture is indicated.

DIFFERENTIAL DIAGNOSIS

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Stool microscopy – darkfield/phase contrast- microscopy is the initial test- shows curved bacilli

Stool gram stain Stool culture with isolation of the organism

and identification of serotype O1 or O139 is the gold standard

colonies appear typically as yellow shiny colonies on thiosulphate citrate bile salt sucrose(TCBS)

DIFFERENTIAL DIAGNOSIS CONT’D

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The goal is: Evaluate patients individually Prompt fluid and salt replacement Prompt treatment

TREATMENT

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Start ORS solution immediately for patients that can drink

Offer the ORS frequently Measure amount drunk and fluid lost in

stool and vomitus= input/output Frequent small sips for patients that vomit/

ORS by NG tubeNB: ORS solution must be prepared with

safe water (boiled or treated with chlorine).

ORAL REHYDRATION

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Amount of ORS (in mls) can be calculated for each patient.

Multiply patient’s weight by 75A rough guide is to give older children and adults

100ml ORS every five minutes until patient is stable. However if more fluid is requested by patient , it

should be given NB: mothers should continue breastfeeding infants

that are affected. Assess patient one hour after commencement of

treatment Thereafter two hourly until rehydration is complete.

GUIDELINE FOR ORAL REHYDRATION

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Approximate amount of ORS solution to give in the first 4 hours to patient with some dehydration.

Use patient’s age where the weight is not known.

Guideline for treating patients with some dehydration

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Age < 4mon

4-11 mon

12-23mon

2-4 yrs

5-14yr

≥15yr

Weight(kg)

<5 5-7 8-10 11-15 16-29 ≥ 30

ml 200-400

400-600

600-800

800-1200

1200-2200

2200-4000

FLUID REQUIREMENT.

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Patients with uncontrollable vomiting, severe dehydration who cannot drink should be rehydrated intravenously

Ringer’s Lactate Solution is the best fluid Normal saline is acceptable, but it does not

correct acidosis Start intravenous fluid immediately If patient can drink , give ORS solution while

i.v drip is set up NB: Give 100ml/kg Ringer’s Lactate Solution

as divided below.

INTRAVENOUS REHYDRATION

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Age First 30ml/kg in

Then 70ml/kg in

Infants(<12mons)

1 hour 5hours

Older(> 1yr)

30mins 21/2 hours

GUIDELINES FOR INTRAVENOUS REHYDRATION

Repeat once if radial pulse is still very weak or. undetectable

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*Standard WHO approved ORS contains Na+ 75, K+ 20,Cl- 65, citrate 10 and glucose 75(all in mmol/L) with osmolality of 245mOsmol/L

Monitor patient closely Reassess the patient 1-2hourly and continue

rehydration If hydration is not improving, give infusion more

rapidly200ml/kg may be required in the first 24hours As soon as patient can drink give ORS solution

(about 5ml/kg/hour

GUIDELINES FOR INTRAVENOUS REHYDRATION CONT’D

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Patient with high rate of purging (e.g.>1L/hour) should be nursed in isolation

Appropriate disinfecting agent must be used to clean up

As soon as patients are able to eat, normal diet should be started.

SUPPORTIVE CARE

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Thirst subsides Pulse is stronger Skin turgor returns Urine has been passed

SIGNS OF REHYDRATION

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Patients with high purging rate benefit from antibiotics

Antibiotic are recommended in moderately and severely ill patients who continue to pass large volume of stool in spite of rehydration.

Oral antibiotic reduce the volume and duration of dirrhoea

Choice of antibiotics should be based on available drugs and individual case consideration

ANTIBIOTICS SHOULD BE GIVEN ORALLY.

ANTIBIOTIC THERAPY

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Classification of patients

First choice Second choice

Adults (non-pregnant)

•Doxycycline:300mg p.o – in a single dose•Ciprofloxacin : 1000mg as a single dose

•Azithromycin 1gm as a single dose•Tetracycline 500mg qds x 3 days•Erythromycin 500mg qds x 3 days

Pregnant women •Azithromycin1gm – single dose

•Erythromycin 500mg qds x 3 days.

Children ≥ 12mons and capable of swallowing pills and oral tablets

•Azithromycin oral suspension 20mg/kg – single dose•Erythromycin 12.5mg/kg qds x 3 days. •Doxycycline 2-4mg/kg- single doseDoxycycline 2-4mg/kg –single oral dose(chidren > 8yrs)

•Tetracycline :12.5mg/kg qds x 3days. (For children > 8yrs)

APPROPRIATE ORAL ANTIBIOTICS

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Classification of patients

First choice Second choice

Children < 12mons old and others unable to swallow pills and /or tablets

•Azithromycin oral suspension, 20mg/kg – single dose•Doxycycline 2-4mg/kg –single oral dose(chidren > 8yrs)

Tetracycline :12.5mg/kg qds x 3days. (For children > 8yrs)

ANTIBIOTICS CONTINUED

ZINC SUPPLEMENTNB: Administration of zinc in children with diarrhoea caused by infection significantly reduces the duration and severity of diarrhoea. It should be taken until recovery. Dose : 10-20mg/day.Zinc opposes the cholera toxin induced electrolyte secretion.

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In developed countries where proper sewage and water treatment exist, cholera is rare except cases related to travel outside the countries

Basic precautions protects from cholera Frequent hand washing with soap especially after using

the toilet and before handling food Use of alcohol based sanitizer if soap is not available Drink safe water- boiled or disinfected Food should be well cooked and eaten hot Avoid food vendors Avoid raw or under cooked sea foods Avoid salads, fruits that can’t be peeled. Avoid dairy products(unpasteurised milk, ice cream)

PREVENTION

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Main goal is to reduce death by Prompt treatment Conyrol spread of the disease Provision of basic amenities( -safe water - proper sanitation - Safe food handling practices

Health education Improved self hygiene

RESPONSE TO OUTBREAK OF CHOLERA

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Two types of oral vaccine are available Both are whole cell killed vaccines Both provide > 50% protection which last for two years. Both are prequalified and licensed by WHO in >60 countries - Dukoral- provides short term protection of 85-90%

against V. cholerae O1Dukoral is given in 150ml of water - Shancol – provides long term protection against V.

cholerae O1 and O139 in children < 5years. Both are given in two doses between 7days and 6 weeks

apartNB: Parenteral vaccine is not recommended by WHO because

its protective efficacy is low and the severe adverse effects associated with it.

CHOLERA VACCINES

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Cholera is an acute diarrhoea disease Spread through contaminated water Causes severe diarrhoea and dehydration Fatal within hour if left untreated Can be successfully treated with ORS in

upto 80% of cases Easily treated Provision of safe water and proper sewage

disposal will reduce the outbreaks oral vaccines are available

KEY FACTS

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THANK YOU