Leptospirosis discussion and CPG

8/14/2019 Leptospirosis discussion and CPG

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Leptospirosis CPG 2010

Angelo P. Ampong, M.D.Emergency Medicine Resident

EAMC


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Leptospirosis

Weil's syndrome

canicola fever

canefield fever

nanukayami fever 7-day fever

Rat Catcher's Yellows

Fort Bragg fever Black jaundice

Pretibial fever


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Incidence

680leptospirosis cases and 40 deaths

from the disease reported every year

prevalence of 10/100,000

It is seasonalwith a peak incidenceduring the rainy months of Julyto

October


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What is leptospirosis?

infectious disease caused by genus

Leptospira

transmitted directly or indirectly fromanimals to humans - ZOONOSIS

Human-to-human transmission occurs

only very rarely


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Philippines: antibodies to various leptospiral

serovars have been reported in: urban domestic rats

rural field rats water buffaloes

cattle

pigs

dogs

monkeys


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Leptospira

corkscrew-shaped bacteria, which differ fromother spirochaetes by the presence of endhooks.

order Spirochaetales family Leptospiraceae

genus Leptospira

too thin to be visible under the ordinarymicroscope

Dark-field microscopy


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Leptospira spp

Two species were recognized:

Leptospirainterroganspathogenic

Leptospira biflexa saprophytic


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What causes the pathological phenomena inleptospirosis?

damage to the endothelial lining of small blood vessels:

interstitialnephritis and tubular, glomerularand vascularkidney lesions leading to uraemia and oliguria/anuria

vascular injury to hepatic capillaries, in the absence ofhepatocellular necrosis, causes jaundice

inflammation of the meninges causes headache, neckstiffness, confusion, psychosis, delirium


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If a patient dies from leptospirosis, what

is the cause of death?

Renal failure

Cardiopulmonary failure

widespread haemorrhage

Liver failure is rare, despite the presenceof jaundice


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What is the outcome of leptospirosis

during pregnancy?

fetal death

abortion

Stillbirth

congenital leptospirosis


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How long is the incubation period?

514 days


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serovar-specificantibodies areprotective

a patient isimmune to reinfection with the

same serovar


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bloodinvade all tissueshost'simmune responseconvoluted

tubules cleared from the kidneys

may persist in the eyes


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Classic Leptospirosis

Septicemic (leptospiremic) phase Lasts a week

fever of sudden onset

chills

severe myalgia

anorexia conjunctival suffusion

nausea

Vomiting

3- to 4-day period of relative improvement

Immune Phase leptospires cannot be cultured from blood


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Weils disease(19thcentury)

fever

jaundice

Splenomegaly

Weils disease

fever

jaundice

renal failure


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CLINICAL RECOGNITION OF

LEPTOSPIROSIS


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2010 CPG

FEVER of at least 2days

AND either :

residingin a flooded area or

has high-risk exposure

wading in floods and contaminated water

contact with animal fluids

swimming in flood wateringestion of contaminated water

(with or without cuts or wounds)

AND presenting with at least two of the following symptoms:

myalgia

calf tenderness

conjunctival suffusionchills

abdominal pain

headache

jaundice

oliguria

should be considered a suspected leptospirosis case


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MILD

Any suspected case with acute febrile illness

BUT with stable vital signs, anicteric sclerae

with good urine output

no evidence of meningismus / meningeal irritation,sepsis / septic shock, difficulty of breathing norjaundice and can take oral medications

considered MILD LEPTOSPIROSIS and can bemanaged on an OUT-PATIENT SETTING


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MOD-SEVERE

Any suspected case with acute febrile illness

unstable vital signs

jaundice/icteric sclerae

abdominal pain

nausea

vomiting and diarrhea

oliguria/anuria

meningismus / meningeal irritation

sepsis / septic shock

altered mental states or difficulty of breathing

Hemoptysis


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LABORATORY DIAGNOSIS OF

LEPTOSPIROSIS


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it is not necessary to confirm the

diagnosis before starting treatment.

Early recognition and treatmentis

MORE important to prevent complications

of the severe disease and mortality


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What are the laboratory findings inpatients with leptospirosis?

elevated erythrocyte sedimentation rate,

thrombocytopaenia leucocytosis

hyperbilirubinaemia

elevated serum creatinine elevated creatinine kinase

elevated serum amylase


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Direct Detection Method1. Culture and isolation remains the GOLD standard BUT is

time-consuming

labor-intensive

requires 6 to 8 weeks for the result

needs darkfield microscopy and has low diagnostic yield. can identify the serovar but is insensitive.

2. Polymerase Chain Reaction (PCR) has the advantage ofearly confirmation

diagnosis especially during the acute leptospiremic phase(first week

of illness) before the appearance of.


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What is the microscopic agglutination test(MAT)?

determines agglutinating antibodies in theserum of a patient by mixing it in variousdilutions with live or killed, formolizedleptospires.

Antileptospiral antibodies present in theserum cause leptospires to stick together toform clumps


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Indirect Detection Methods

1. Microagglutination Test (MAT)

a four-fold rise of the titer from acute to

convalescent sera is confirmatory of thediagnosis.

highly sensitive and specific

time-consuming and hazardous (risk ofexposure to the live antigen)

Cross-reaction


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2. Specific IgM Rapid Diagnostic Tests

LeptoDipstick, Leptospira IgM ELISA

(PanBio), MCAT and Dridot

Leptospira genus-specific IgM

sensitivity : 63%-72%

specificity : 93%-96% when tested in illnesses of

less than 7 days.

If serum samples are taken beyond 7 days,

sensitivity improves to > 90%.

false negative results - early stage of the illness


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Nonspecific Rapid Diagnostic Tests

like LAATS (Leptospira Antigen-

Antibody Agglutination Test

(Leptospira Serology Bio-Rad) Leptospira antibody

used as a screening test but is NOT

sensitive.A positive result should be confirmed with

MAT


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1. Complete blood count (CBC) leukocytosis with neutrophilia.

Thrombocytopenia is common.

Platelet count < 100,000/cu mmrisk factor for bleeding and pulmonary hemorrhage

2. Urinalysis proteinuria

pyuria

hematuria Findings may sometimes be mistaken for UTI.

3. Serum creatinine increasing impending acute kidney injury

4. Serum creatine phosphokinase (CPK-MM) elevated severe myalgia.

5. Liver function tests Bilirubin, ALT, AST, and alkaline phosphatase Elevated

6. Bleeding parameters (Prothrombin time, partial thromboplastin time PTT) may be prolonged.


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SEVERE

1. Complete blood count (CBC) leucocytosis (WBC>12,000 cells/cumm) with neutrophilia and thrombocytopenia ( 3 mg/dL (or CrCl < 20 ml/min) and BUN > 23 mg/dL

3. Liver function tests - AST/ALT ratio > 4x, Bilirubin > 190 umol/L

4. Bleeding parameters - prolonged prothrombin time (PT) < 85%

5. Serum potassium > 4 mmol/L

6. Arterial blood gas (ABG) severe metabolic acidosis(ph< 7.2, HCO3 < 10)

and hypoxemia (PaO2 < 60 mmHg, SaO2 < 90%, PF ratio


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TREATMENT OF LEPTOSPIROSIS


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MILD leptospirosis Doxycycline

amoxicillin and azithromycin

MODERATE -SEVERE leptospirosis

Penicillin G

ampicillin, 3rd generation cephalosporin(cefotaxime, ceftriaxone), and

parenteral azithromycin


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Jarisch-Herxheimer reactions have been reported in patients withleptospirosis treated with penicillin.

release of heat-stable proteins from spirochetes

release of endotoxins occurs faster than the body can remove the toxins.

It manifests as fever, chills, rigor, hypotension, headache, tachycardia,hyperventilation, vasodilation with flushing, myalgia and exacerbation ofskin lesions.

Reaction commonly occurs within two hours of drug administration, but isusually self-limiting.

inflammatory process results from activation of the cytokine cascade duringthe degeneration of spirochetes tumor necrosis factor alpha

interleukin-6

interleukin-8


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Antibiotic therapy should be completed

for 7 days, except for azithromycin


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Antibiotic therapy should be started as soonas the diagnosis of leptospirosis is

suspected regardless of the phase of

the disease or duration of symptoms


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PROPHYLAXIS FOR LEPTOSPIROSIS


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PRE-EXPOSURE PROPHYLAXIS

The most effective preventive measure isavoidance of high-risk exposure

(i.e. wading in floods and contaminated

water, contact with animals body fluid).


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Pre-exposure antibiotic prophylaxis is

NOT ROUTINELY RECOMMENDED


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Doxycycline200 mg once weekly, to

begin 1 to 2 days before exposure and

continued throughout the period ofexposure.


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There is NOrecommended pre-exposureprophylaxis that is safe for pregnant and

lactating women.


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POST-EXPOSURE PROPHYLAXIS

LOW-RISK EXPOSURE

singlehistory of wading in flood or contaminated water without wounds,cuts or open lesions of the skin.

Doxycycline 200 mg single dose within 24 to 72 hours from exposure

MODERATE-RISK EXPOSURE

singlehistory of wading in flood or contaminated water and the presenceof wounds, cuts, or open lesions of the skin

OR

accidental ingestion of contaminated water

Doxycycline 200 mg once daily for 3-5 days to be started immediatelywithin 24 to 72 hours from exposure


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HIGH-RISK EXPOSURE continuous exposure

residing in flooded areas, rescuers and reliefworkers, wading in flood or contaminated water

with or without wounds, cuts or open lesionsof the skin.

Swimming in flooded waters infested withdomestic/sewer rats

ingestion of contaminated water

Doxycycline 200 mg once weekly until the end ofexposure


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LEPTOSPIROSIS ASSOCIATED AKI


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Pathophysiology


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OLIGURIA

Oliguria is defined as urine output < 0.5mL/kg/hror


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DIALYSIS

Any one of the following is an indication for dialysis:

Uremic symptomsNausea, vomiting, altered mental status, seizure, coma

Serum creatinine > 3mg /dL

Serum K > 5 meq /L in an oliguric patient

ARDS, pulmonary hemorrhage

pH < 7.2

Fluid overload

Oliguria despite measures following the Oliguria algorithm

individually or collectively they should indicate early dialysis


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Presence of uremic symptoms is anabsoluteindication for dialysis


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non-oliguric renal failure with mildhypokalemia

Oliguriawith hyperkalemiapoor

prognosis


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Oliguria -


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Furosemide 40 mg IV bolus

Urine Output>0.5 mL/kg/hr?

Yes

Monitor hourly

and adjust rate of

IVF to maintain

euvolemiaNo

Double dose of furosemidehourly up to a maximum of 160 mg

Yes

Urine Output

>0.5 mL/kg/hr?

No

Acute Renal Replacement Therapy


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PULMONARY COMPLICATIONS OF

LEPTOSPIROSIS


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Tachypnea (Respiratory Rate > 30/min) isthe first sign of pulmonary involvement

in most cases.


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Consider lung involvement with the onsetof cough, hemoptysis or dyspneain a

patient with a clinical diagnosis of

leptospirosis


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Pulmonary symptoms usually appearbetween the 4thand 6thday of disease


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Most Common Complications

Pulmonary hemorrhage

Acute Respiratory Distress Syndrome


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PULMONARY HEMORHAGE

disruption of the vascular endotheliumwould lead to an increase in

permeability, which would in turn give

rise to alveolar bleeding. hemoptysis

alveolar infiltrates (CXR)


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Bolus methyl prednisolone given withinthe first 12 hours of onset of respiratory

involvement is life saving

Methylprednisolone:1gm IV/day for 3

days

followed by oral Prednisolone 1mg/kg/day for 7 days


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THANK YOU!


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Renal failure

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Leptospirosis discussion and CPG

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