Leptospirosis is a bacterial disease that affects humans and animals. It is caused by bacteria of the genus Leptospira. In humans, it can cause a wide range of symptoms, some of which may be mistaken for other diseases. Some infected persons, however, may have no symptoms at all.
Case study of a 22 year old male patient admitted under medics with an unknown disease process, likely infectious with unknown causative agent. Extensive investigation revealed leptospirosis. Presented at hospital lunchtime medical meeting. These slides have been altered to ensure patient anonymity, and to better display information without a presenter.
Sources for all imagery and sources listed in references section where possible. I do not claim ownership of any images or graphics. Slides for educational purposes only, and should not replace clinical judgement. No monetary gain was made for this work.
Proper Case Presentation for Dengue Fever, Prevention, Treatment and everything else. Prepared by Dr Zain Khan, Doctor at Liaquat College of Medicine and Dentistry
CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC EN...Akhil Joseph
A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.
Case study of a 22 year old male patient admitted under medics with an unknown disease process, likely infectious with unknown causative agent. Extensive investigation revealed leptospirosis. Presented at hospital lunchtime medical meeting. These slides have been altered to ensure patient anonymity, and to better display information without a presenter.
Sources for all imagery and sources listed in references section where possible. I do not claim ownership of any images or graphics. Slides for educational purposes only, and should not replace clinical judgement. No monetary gain was made for this work.
Proper Case Presentation for Dengue Fever, Prevention, Treatment and everything else. Prepared by Dr Zain Khan, Doctor at Liaquat College of Medicine and Dentistry
CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC EN...Akhil Joseph
A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.
Case Study on Reteropositive with RF,LRTI,UTI and Sepsis .pptxKamaljeet ..
Case study on Reteropositive with LRTI with Respiratory Failure with UTI with SEPSIS
for Pharmacotherapeutics-II
Department of Pharmacy Practice
(PharmD)
Irritable bowel syndrome is a common condition affecting the digestive system.
Symptoms of irritable bowel syndrome include stomach cramps, bloating, diarrhoea and constipation. These may come and go over time.
Making changes to your diet and lifestyle, like avoiding things that trigger your symptoms, can help ease irritable bowel syndrome.
blockage or problem in the urinary tract can mean urine is unable to drain from the kidneys or is able to flow the wrong way up into the kidneys. This can lead to a build-up of urine in the kidneys, causing them to become stretched and swollen.
An injury higher on the spinal cord can cause paralysis in most of your body and affect all limbs (tetraplegia or quadriplegia). A lower injury to the spinal cord may cause paralysis affecting your legs and lower body (paraplegia)
Scoliosis is the abnormal twisting and curvature of the spine. It is usually first noticed by a change in appearance of the back. Typical signs include: a visibly curved spine. one shoulder being higher than the other.
Osteoarthritis (OA) is the most common form of arthritis. Some people call it degenerative joint disease or “wear and tear” arthritis. It occurs most frequently in the hands, hips, and knees.
With OA, the cartilage within a joint begins to break down and the underlying bone begins to change. These changes usually develop slowly and get worse over time. OA can cause pain, stiffness, and swelling. In some cases it also causes reduced function and disability; some people are no longer able to do daily tasks or work.
About 4 out of 5 cases of acute pancreatitis improve quickly and don't cause any serious further problems. However, 1 in 5 cases are severe and can result in life-threatening complications, such as multiple organ failure. In severe cases where complications develop, there's a high risk of the condition being fatal.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
3. C.R.
18 yrs old
Sitio Sagur Pugaro Suit Dagupan city
Single
Oct. 7, 1999
Roman Catholic
Admitted at R1MC for the first time
Informant : Mother
Realiability : 90 %
6. 3 days
DAY 1 ILLNES
• + undocumented fever, + myalgia, Headache
• + Abdominal pain, +Dec appetite and activity
• Took Paracetamol 2X, no consultation done
2 days
DAY 2 ILLNES
•+ persistence of above S/SX
•↓ urine output with yellow orange in color
•+ calf pain
1 WEEK HISTORY OF WADING TO FLOOD
7. 1 day
•+ persistence of above S/SX
•LBM and vomiting
•Last urine output: 12noon < 1ml
Few hrs
•+ anuria
•+DOB
•Sought consult to R1MC
10. Past medical history:
EPI Completion
No pertinent childhood illnesses
No previous surgical interventions
Family history:
No history of herediofamilial diseases
No history of TB, asthma, DM and cardiac disease.
11. Personal and Social History:
Patient is staying with his father and 2
siblings in a Well- lit, well ventilated
bungalow wooden house with own pour-
flush toilet.
Garbage collected 2-3 times a week
Drinking water is tap water
No history of travel
12. H- The patient lives with his father with his 2
siblings (his parents are separated)
E- He stop schooling at Grade 10
A- He accompanies his father during fishing and
usually play basketball during free time.
D- No history of illegal drugs. Usually drinks SAN
MIG light with his friends and a smoker as well.
S- No sexual experience
S- No suicidal Ideation
13. Awake, conscious, coherent, ambulatory, GCS
15, in cardiorespiratory distress with the
following vital signs:
BP: 50/30
PR: 98bpm
CR: 85bpm
Temp: 37C
14. SKIN:
Brown in complexion, no pallor, mild jaundice, no
lesions, normal skin turgor, multiple scars on bilateral
lower extremities
HEENT:
No areas of balding, no swelling, tenderness
EYES: pale palpebral conjunctivae, icteric sclera,
conjunctival suffusion, no cataract, no asymmetry
EARS: at level of lateral canthus of the eyes,
symmetrical, non-tender, with no erythema, no
discharges, no scaling
NOSE: Nasal mucosa is pink, patent nares, non-
deviated septum and no Nasal discharge, non-
tendersinuses.
15. MOUTH: pinkish lips, Buccal mucosae is pink,
no ulcer, Dry lips
CHEST AND LUNGS:Symmetrical chest wall
expansion,No intercostal or subcostal
retraction,no tenderness, normal resonant
breathing sound,
Heart: Adynamic precordium, Apex beat at 5th
ICS left MCL, , (-) thrills, (-) loud and palpable
P2; normally split S2; (-) S3, (-) S4.normal rate.
(-) murmur, tachycardic.
16. Abdomen.
Inspection:, no scars, no spider angioma
Auscultation: hypoactive bowel sounds at 6 per minute.
Percussion: Tympanic, liver span 8 cm in right
midclavicular line, non palpable liver edge.
Palpation: (-) tenderness
Musculoskeletal: (+) tenderness Gastrocnemius, No bone
nor joint deformity, no joint swelling
Extremities: full pulses, warm extremities, CRT 2 seconds,
no cyanosis, no edema
Neurologic: Conscious, coherent, oriented to three spheres,
follows commands
GCS 15 (E4V5M6)
The rest of the neurologic examinations were
unremarkable
17. SUBJECTIVE OBJECTIVE
18 years old
Male
History of wading in flood
Fever for 3 days
Headache
Decreased urine output
for 2 days
Vomiting and Loose
Stools
Abdominal Pain
Calf Pain
Hypotension (BP 50/30)
Tachycardia (CR: 115bpm)
Signs of Dehydration (dry
lips)
Icteric Sclera
Conjunctival suffusion
Multiple scars on lower
extremities
Tenderness on
Gastrocnemius
19. HD/PICU DAY 1:
3:40 pm
Patient was admitted at Pediatric ICU under GREEN
service
Secure consent
Diagnostics: CBC, typings, BUN , Crea, S. Electrolytes,
AST, ALT, PT APTT, blood cs, U/A, dengue test,
leptospira test, CXR PAL
Therapeutics
Line 1: PNSS 1L TRA 52gtts/ min x 6hrs then refer for
RA
Line 2:PNSS 1L TRA 22gtts/,in x 24 hrs (M%)
20. Penicillin 2million units Q4 (-)ANST
Please insert IFC
Refer to nephro
Monitor vs q1
Monitor I and O q shift
Hook to norepinephrine 31cc + D5w 69cc with
rate of 5
For possible HD explained to mother
Hook to o2 via face mask via 10 LPM
Give dopamine drip at 10 cc / hr
21. 5:40pm
BP: 110/50
(-) urine output
10:30pm
please give metolazone 5mg now, then furosemide 4mg
IVP after 1 hr of giving metolazone
HD/PICU DAY 2 : Nephrology Notes
BP: 100/50 (+) Neck vein distention (-) desaturation
give furosimide 80mg now
for hep B and C
PICU notes
Line 1 please regurate to PNSS 22gtts/min as maintenace
Line 2 shift to heplock
22. 12pm :
(+) Tachypnea
For “E” intubation, conditioned well explained to
patient
For repeat CXR APL
23. HD/PICU DAY 2 :
labored breathing, + distention neck vein , GCS
15 , + crackles
IVF: PNSS 1 L TRA 22 gtts/min
O2 via face mask at 10 LPM
for “E” intubation (refused)
Meds: Pen G
Norepinephrine drip @ 5cc/hr
Dopamine drip @ 10cc/hr
For hemodialysis once IJ cath is secured
For IJ cath insertion
24. TCVS notes
S/P femoral cath insertion
May proceed to HD
1:45PM
HD order: duration 2hrs
blood flow 25ml per min
dialysate flow 400 per hr
Ultrafiltrate 500 per hr
Follow up hepatitis profile
2:33 Pm
+ desaturation
cr=20s
rr=30s fair pulses warm extremeties
CPR STARTED with 5 cycles
3:10: pronounced clinically dead
28. Human leptospiral infections can occur when
mucus membranes and skin are contaminated
by the urine of infected animals, or upon
ingestion of contaminated food and water.
Rat is the principal source of human infection.
Leptospirosis is endemic in the Philippines and
the number of cases peak during the rainy
months of June to August. Outbreaks have
been associated with wading in flood waters.
29. most important
zoonotic disease in the
world
Leptospira sp. - obligate
aerobic, motile tightly
coiled spirochetes
23 pathogenic
species
8 non-pathogenic
species
LEPTOSPIROSIS
30. Reservoir: rodents
Transmission:
direct contact (blood, tissues, organs or
urine of infected animals)
indirect contact (injured mucosa or
skin is exposed to contaminated water
or soil)
LEPTOSPIROSIS
31. Common in tropical and subtropical
countries
The median incidence
20.6 among males < 19 years of age
6.8 in females (10 – 19 years of age)
Increasing incidence in the Philippines
2,495 cases in 2017 (49.1% higher)
234 cases from Jan to Jun 2018 (16% higher)
LEPTOSPIROSIS
32. Leptospires enter human through moist and
abraded skin or mucous membranes
Circulate in the bloodstream
Primary lesion is damage to the
endothelial lining of small blood vessels with
ischemic damage to the liver, kidneys, meninges
and muscles.
33.
34. Incubation period 2 to 20 days (mean: 15
days)
Varied manifestations
Severity of Illness:
Asymptomatic or subclinical self-limited
febrile systemic illness (90%)
Life-threatening illness - jaundice, renal
failure myocarditis, hemorrhage, and
refractory shock (10%)
CLINICAL MANIFESTATIONS
Handbook of Pediatric Infectious Diseases. Philippine Pediatric Society. 2014 Edition.
35. ANICTERIC LEPTOSPIROSIS
initial or the SEPTICEMIC PHASE
Abrupt with fever, chills, severe headache, malaise,
nausea, vomiting, severe muscular pain and tenderness.
Conjuctival suffusion with photophobia and orbital pain
w/o chemosis and purulent exudate.
Hepatosplenomegaly, generalized lymphadenopathy.
Truncal red maculopapular rash
Second or immune phase follows a brief asymptomatic
interlude with recurrence of fever (bi phasic)
Aseptic meningitis
36. Icteric / Weil’s Syndrome
Severe form affecting < 10 % of children
Hemorrhage and Cardiovascular collapse
RUQ pain, hepatomegaly, inc. liver enzymes,
hyperbilirubinemia
Azotemia Oliguria ANURIA
37. Clinical features associated with increased risk
for mortality :
altered mental status,
respiratory insufficiency (rales, infiltrates),
hemoptysis,
oliguric hyperkalemic acute renal failure,
and cardiac involvement (myocarditis,
complete or incomplete heart block, atrial
fibrillation).
38.
39.
40.
41.
42.
43.
44.
45.
46. If children are exposed for more than 7 days,
the dose should be repeated after 1 week.
Prophylaxis is not 100% effective. Prevention of
exposure is most prudent. Monitor all those
exposed for the occurrence of symptoms of
leptospirosis. The early signs of infection occur
between 4 and 10 days after exposure
47. All patients with a presumptive diagnosis of
Leptospirosis will be triaged under the
Department of Pediatric Nephrology (Patients
< 18 yo) with the following criteria:
1. Serum Creatinine : > 3 mg/ dl
2. Presence of any ONE of the Criteria for Pulse
Therapy (See Appendix II)
48.
49.
50.
51. Indications for acute renal replacement
therapy or dialysis
Uremic Symptoms
Serum creatinine > 3mg/dL
Serum K > 5 meqs/L in an oliguric patient
ARDS, Pulmonary hemorrhage
pH <7.2
Fluid overload
Oliguria
RENAL REPLACEMENT THERAPY
52. Hemodialysis is preferred over peritoneal dialysis
Hemodialysis - faster way of removal of toxins
Hemodialysis versus Peritoneal Dialysis
mortality (0 vs 10 %)
renal recovery time (8.3 days vs. 16.2 days)
reduction of serum bilirubin, urea, and creatinine
RENAL REPLACEMENT THERAPY
Wiwanitkit V. (2006). Comparison between blood exchange and classical therapy for
acute renal failure in Weil’s disease: appraisal on Thai reports. Nephrology
(Carlton);11(5):481.
53.
54.
55.
56.
57. Incidence: 20 - 70%
Consider if with: cough, hemoptysis,
dyspnea
Pulmonary symptoms usually appear
between the 4th and 6th day of illness
Pulmonary hemorrhage and Acute
Respiratory Distress Syndrome are
most common
Gouveia, E.L, Metcalfe, J., de Carvalho, A.L.F., Aires, T.S.F., Villasboas-Bisneto, J.C., Queirroz, A., Santos, A.C., Salgado, K., Reis, M.G., and
Ko, A.I. Leptospirosis-associated Severe Pulmonary Hemorrhagic Syndrome, Salvador, Brazil. Emerging Infectious
Diseases • www.cdc.gov/eid • Vol. 14, No. 3, March 2008
61. 1. Parents should instruct children not to wade
or swim in flood waters.
2. If exposure to flood waters is unavoidable,
protective gear such as boots, goggles, overalls,
and rubber gloves should be used.
3. All food and drinking water should be
protected against contamination. Fresh
vegetables and fruit should be washed in
previously boiled or clean water and then
cooked or peeled.
.
62. 4. Boil drinking water for at least 10-15 minutes.
Physical filtration through ceramic orcharcoal
filters is not adequate for leptospirosis.
5. Food should be protected against rodent attack
or contamination.
6. If children are exposed to flood waters, antibiotic
prophylaxis may decrease occurrence of clinical
disease and mortality. Prophylactic antibiotics
should be given under the supervision of a
physician, who can give advice regarding effects,
precautions and contraindications for these
medications.
Editor's Notes
The most important and most common zoonosis, caused by infection with pathogenic spirochetes of the genus Leptospira
The reservoir are mainly rodents
Transmission to man occurs through direct contact with blood, tissues, organs, or urine of infected animals, or through indirect contact, when injured mucosa or skin is exposed to contaminated water. In tropical countries, leptospirosis is an endemic disease, with outbreaks occurring during the rainy season, coinciding with flooded areas.
There is increasing incidence of leptospirosis in the Philippines, In 2017, A total of 2,495 leptospirosis cases were reported nationwide from Jan. 1 to Dec. 2, 2017. This figure was 49.1 percent higher than the 1,673 cases recorded during the same period in 2016.
At present, a total of 234 leptospirosis cases were recorded compared to last year's 146 cases, covering January 1 to June 29.
Clinical presentation may be mono- or biphasic. Classically described biphasic leptospirosis has an acute SEPTICEMIC PHASE usually lasting 1 week, during which time Leptospira organisms are present in blood, CSF and all other tissues, and the IMMUNE PHASE which lasts 4 to 30 days during which leptospiuria is evident.
The acute phase is characterized by nonspecific symptoms, including fever, chills, headache frequently frontal in distribution, myalgia, nausea, vomiting, abdominal pain, and conjunctival suffusion, occasionally accompanied by rash. Distinct clinical findings include notable conjunctival suffusion without purulent discharge (28%–99% of cases) and myalgia of the calf and lumbar regions (40%–97% of cases).
Incubation period is 2-20 days with mean of 15 days
Severity of illness vary from Asymptomatic or subclinical self-limited febrile systemic illness (90%) to Life-threatening illness - jaundice, renal failure myocarditis, hemorrhage, and refractory shock (10%)
The following are the indications for renal replacement therapy
In our patient elevated serum creatinine, pulmonary hemorrhage and oliguria are the indications
Hemodialysis is preferred over peritoneal dialysis
Hemodialysis - faster way of removal of toxins
Hemodialysis versus Peritoneal Dialysis
mortality (0 vs 10 %)
renal recovery time (8.3 days vs. 16.2 days)
reduction of serum bilirubin, urea, and creatinine
Tachypnea (Respiratory Rate > 30/min) is the first sign of pulmonary involvement in most cases. One should consider lung involvement with the onset of cough, hemoptysis or dyspnea in a patient with a clinical diagnosis of leptospirosis.
Pulmonary Complications occur in 20-70% of patients
Usually presents with cough, hemoptysis, dyspnea on the 4th and 6th day of illness
Such in our case
Pulmonary hemorrhage and Acute Respiratory Distress Syndrome are most common
Significant risk factors for pulmonary complications are delayed antibiotic treatment and thrombocytopenia at the onset of the disease.
The pathogenesis is not clearly defined although vascular endothelial involvement has been demonstrated to occur through an immunologic mechanism in which the toxin acts as an antigen. The disruption of the vascular endothelium would lead to an increase in permeability, which would in turn give rise to alveolar bleeding