CASE with high grade fever 10 day,R/sided pleuritic type

CASE  1

A PATIENT WITH POORLY RESOLVING LUNG ABCESS

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(PULMONARY MELIOIDOSIS)

•      NAME-Mr. L.Nadaraja

•      60 yrs old patient

ADRESS-NO-28,MOHOMAD ASIF ROAD,

                       
AKKAREIPATHTHUWA

•      Admitted on
2017/07/28- to ward 14

•      DOA-2017/07/28

•      DOD-2017/08/18

•      BHT-31082

 

Candidate

Dr.H.K.D.K.Prabasara

Superviser

Dr.Prasanna Wijerathna

(consultant respiratory physician,

DGH-ampara)

SUMMARY

60 years old L.Nadaraja ,poorly controlled diabetic patient from
akkareipaththuwa was transferred from BH-Akkareipaththu for the management of
poorly resolving R/sided lung abcess.patient  was initially presented them with high grade
fever 10 day,R/sided pleuritic type chest pain for 14days with radiological
evidence of lung abcess.For that they have treated with IV-Cefotaxime.Because
of poor resolution of the abcess despite of treatments they transferred the
patient to DGH-Ampara.On admission to our ward patient was clinically  ill looking with high grade fever spikes.On
admission he was tachypnoic with clinical evidence of R/sided pneumothorax.Pulse
rate was 130/min and blood pressure was maintained.CXR taken on admission
revealed R/sided pneumothorax with evidence of R/midzone lung abcess.IC tube
was inserted and treatment started with IV-clindamycin lung abcess.Two days following
IC tube insertion patient developed significant surgical emphysema which was
extending below to abdomen and upto abdomen and repeat CXR revealed
pneumomediastinum with pneumopericardium.This could be related to IC-tube insertion
or perforation of abcess in to mediastinum ,pericardium or bronchopleural
fistulae and this was managed conservatively with oxygen via face
mask.Considering underlying diabetes with poor clinical respond to antibiotics
treatments started for melioidosis while awaiting for melioidosis serology
report.IV merophenum and co-trimoxole started and melioidosis antibody was
traced and it was highly positive with 1:12000 titre.Patient was well responded
to Merophenum and cotrimoxole with very significant clinical and radiological
improvement.Considering the right sided hilar prominence bronchoscopy was done
and it was negative. IV –merophenum was given for two weeks and patient was
discharged on oral co-trimoxole and oral hypoglycaemic agents and planned to continue
co-trimoxole for 6 month duration.

HISTORY

This
patient was transferred from BH-Akkareipaththu for management of poorly
resolving  lung abcess R/mid zone after
treating with IV-cefotaxime 1g tds for 7days.

He
had a history of fever for 10 days,R/sided pleuritic type chest pain and cough
for 14 days duration.Fever was high grade fever and associated with chills and
rigors which was not responded to paracetamol.Cough also was a mild cough for
14 days which was not triggered with cold wheather or cold foods .it was a
productive and sputum was yellowish and scanty while poorly responded to
salbutamol nebulization.

R/Sided
chest pain was persistent as a mild pain but It was increased with coughing and
with deep inspiration,and it was not consisted with ischaemic features.

He had loss of appetite and lost his weight for
last one month duration.there was no history of haemoptysis .He does not have a
positive contact history with tuberculosis patient.

 

 

PAST MEDICAL HISTORY

Patient is a poorly controlled diabetes patient
for last five years.No past history of HTN,dyslipidaemia,IHD.No previous
history of tuberculosis.

PAST SURGICAL HISTORY

Not significant

DRUG HISTORY

He was on metformin 500mg bd,gliclazide 40mg bd

ALLERGIC HISTORY

Not known allergies to food or drugs

FAMILY HISTORY

No family history of bronchial asthma or significant
medical conditions.

SOCIAL HISTORY

He is a threewheel driver and part time farmer
culticating pady. He usesd to take alchohol occasionally and not a smoker.

Family consist of his wife,3 sons and two
daughters,supporting him very much.

EXAMINATION

He was ill looking ,febril to touch and
pale,throat was normal,he was not icteric ,there was no lymphadenopathy or
clubbimg.

RESPIRATORY SYSTEM EXAMINATION

He was dyspnoic RR-25/min and chest movements
was reduced on R/side of the chest ,trachea was centrally located and apex beat
felt 5th ICS mid clavicular line .vocal fremitus was reduced on
R/side of the chest specially toward lower zone posteriorly.R/side of the chest
was resonance compared to left posteriorly.air entry was abcent in R/lower zone
and reduced toward upper zone of the chest posteriorly and air entry was
reduced anteriorly also in R/chest.left lung was normal in examination

CARDIOVASCULAR SYSTEM EXAMINATION

Pulse rate 130/min and regular.blood pressure
100/60 .there was no murmurs or added sounds

ABDOMINAL EXAMINATION

Abdomen was soft and mild R/hypochondriac
tenderness was there.no hepato/splenomegaly ao free fluids in the abdomen

CNS

He was conscious rational and CNS examination
was normal

 

 

 

 

 

Differential
diagnosis

1)R/sided
lung abcess complicated with pneumothorax

2)pulmonary
tuberculosis complicated with pneumothorax

3)melioidosis
complicated with pneumothorax

4)R/sided
lung malignancy +post obstructive pneumonia complicated with pneumothorax

 

 

 

 

 

 

 

 

 

 

 

 

CXR-taken at BH akkareipaththu 2017/07/25

 

 

 

CXR-on admission to DGH-ampara 28/07/2017

 

 

FBC

 

07/28

07/30

08/03

08/05

08/06

08/08

08/15

08/18

Wbc/dc

14000

16000

14000

10000

9500

8600

7200

7400

Neu%

84

88

85

70

68

65

65

64

Lym%

12

9

12

25

26

30

30

32

Eosino%

3

2

2

3

3

3

3

3

Hb

8.9

8.5

8.3

8.5

8.4

8.5

8.7

8.9

platelet

417

560

600

540

360

370

380

354

CRP(mg/dl)

07/28

07/30

08/03

08/05

08/06

08/08

08/15

08/18

168

180

258

190

168

79

32

6.8

ESR mm 1st hour

07/28

08/06

08/12

08/18

68

90

84

56

Melioidosis antibody

08/01

08/08

08/17

 

+ 1:12000

+1:10000

+ 1:780

 

Capillary blood sugar monitored before meal.

Sputum three early morning samples was negative
for AFB

MANTOUX TEST-negetive(5mm)

Sputm gram stain –organisms not seen

Blood picture (08/06)

Normochromic normocytic anaemia with
leucocytosis may be due to acute infection .acute blood loss need to be
excluded

Stool for occult blood

Negative for occult blood

Sputum culture+ABST—no growth

Blood culture+ABST—no growth

Renal function tests

 

07/28

07/30

08/03

08/05

08/06

08/08

08/15

08/18

s.creat

0.6

0.6

0.8

0.9

0.8

0.7

0.7

0.7

B.urea

18

22

24

23

17

18

15

17

Sodium

142

140

136

145

140

139

136

139

Potassium

3.8

3.3

4.0

3.8

3.7

3.9

3.6

3.5

Liver functions

 

07/28

08/03

 

08/15

 

08/18

SGOT

34

38

 

37

 

40

SGPT

18

17

 

20

 

17

ALP

210

228

 

220

 

236

T.PRN

6.8

6.69

 

6.7

 

6.6

ALBUMIN

3.6

3.5

 

3.48

 

3.5

 

Differential diagnosis

1)R/midzone lung abcess complicated with pneumothorax

2)melioidisis

3)pulmonary tuberculosis

4)lung malignancy with post obstructive
pneumonia

 

MANAGEMENT

Patient was managed in the ward with close
monitoring of vital parameters,SPO2 ,input/out put,QHT.

Emperically he was started on IV clindamycin
600mg 8hrly .

Since there was a symptomatic pneumothorax
>2cm rim on CXR intercostals tube was inserted.

Since patient was dyspnoic oxygen was given via
face mask.

Considering poor blood sugar control with oral
hypoglcaemics e insulin was started to a sliding scale and oral drugs withheld.

He was nebulized with salbutamol +normal saline
4hourly for symptomatic relief.

Two days after IC tube insertion (30/07)after
intercostal tube insertion significant surgical emphysema was detected which
was extending up to abdomen and neck.Urgent CXR showed pneumomediastinum
,pneumopericardium with surgical emphysema.Urgent HRCT chest was done it also
revealed  pneumomediastinum and
pneumopericardium with some R/sidede residual pneumothorax.

 

 

Since the intercostal tube was in the correct
position and functioning surgical emphysema, pneumomediastinum and
pneumopericardium was conservatively managed with oxygen to facilitate the
absorption.

Neck and chest girth was monitored.

Even after 3days of IV clindamycin high grade
fever spikes was  persist while sputum
three sample and mantoux was negative.

At this point CRP’s first differential diagnose
was melioidosis and considering patient was critical ill with complicated
pneumothorax,pneumomediastinum and pneumopericardium while awaiting meliodosis
antibody report he was empirically started on IV merophenum 1g t.d.s. and  oral co-trimazole 960mg b.d

After one week over the phone melioidosis
antibody report was traced and it was strongly positive with highly suggestive
of melioidosis.IV clindamycin was stopped and IV merophenum and co-trimazole
continued

After 2 days of starting IV merophenum and
co-trimazole patient was afebrile

Surgical emphysema was settling with improving
neck and chest girth and repeate CXR after 3days pneumomediastinum was absorbed
while pneumothorax was settled.

Intercostals tube was removed(08/05) after
trial of clamping tube for 4hours and tight dressing applied.

Haemoglobin dropped to 6.4mg/dl and 2pint of
blood was transfused.stool for occult blood was negative ,blood picture was
normochromic normocytic anaemia and acute bacterial infection causing low Hb
after excluding acute blood loss.

IV merophenum continued for 21 day to
complete,and considering patients clinical biochemical and radiological
improvement patient was discharged and planned to continue co-trimazole for
minimum 6month duration

 

 

 

 

 

 

DISCUSSION

MELIOIDOSIS

•       Melioidosis is an
infection caused by the facultative intracellular gram-negative bacterium, Burkholderia
pseudomallei . This organism is a widely distributed environmental saprophyte
in soil and fresh surface water in endemic regions .

•       Melioidosis occurs
predominantly in Southeast Asia, northern Australia, South Asia (including
India), and China . The majority of diagnosed cases are from Thailand ,
Malaysia, Singapore , and northern Australia

•      Transmission
 — Transmission of infection can occur via percutaneous inoculation,
inhalation, aspiration, and occasionally ingestion.  Cases of pneumonia following presumptive
inoculating skin injuries are well documented, suggesting that the organism can
reach the lungs via the hematogenous route

•      Risk factors
 — Fulminant melioidosis can occur in healthy individuals, though
severe disease and fatalities are uncommon in those without defined risk
factors . The most important risk factors for melioidosis are diabetes,
hazardous alcohol use, and chronic renal disease

•      Incubation period
 — The incubation period following inoculating injury ranges from 1
to 21 days (usually 1-5 days)

•     
Localized form

Bacteria enter the skin through a laceration or abrasion, and a
local infection with ulceration develops. The incubation period is 1-5 days.
Swollen lymph glands may develop. Bacteria that enter the host through mucous
membranes can cause increased mucus production in the affected areas.

•     
Pulmonary form

When bacteria are aerosolized and enter the respiratory tract via
inhalation or hematogenous spread, pulmonary infections may develop. Pneumonia,
pulmonary abscesses, and pleural effusions can occur. The incubation period is
10-14 days. With inhalational melioidosis, cutaneous abscesses may develop and
take months to appear.

•     
Septicemia

•     
When bacteria is disseminated in the bloodstream in glanders, it is
usually fatal within 7-10 days. The septicemia that develops affects multiple
systems, and cutaneous, hepatic, and splenic involvement may occur. With
melioidosis, bacteremia is observed with chronically ill patients (eg, patients
with HIV, patients with diabetes). They develop respiratory distress,
headaches, fever, diarrhea, pus-filled lesions on the skin, and abscesses
throughout the body. Septicemia may be overwhelming, with a 90% fatality rate
and death occurring within 24-48 hours.

        
Chronic form

          The chronic form
involves multiple abscesses, which may affect           the liver, spleen, skin, or muscles.
This form also is known as farcy in glanders disease. Melioidosis, in addition
to this chronic form, can become reactive many years after the primary infection.

Mortality/Morbidity

The mortality rate in the pulmonary form of glanders is 90-95% if
untreated and 40% if treated. The mortality rate in the septicemic form of
glanders is greater than 95% if untreated and 50% if treated. The mortality
rate in the cutaneous form of glanders is 90-95% if it becomes systemic and if
untreated but 50% if properly treated. For the chronic form of glanders, the
mortality rate may be 50% despite treatment.

Melioidosis has had a reported mortality rate up to 90% if disseminated
septicemia is present. In Australia, the mortality rate is 19%, whereas in
Thailand it is 50%. It is most widespread in Thailand, where in one hospital,
it was responsible for 19% of community-acquired sepsis and 40% of deaths from
community-acquired septicemia. 13 The
fatality rate of melioidosis is greater in people with specific comorbidities,
such as diabetes mellitus, renal dysfunction, or chronic pulmonary disease, and
in people who are immunosuppressed for one reason or another.

Possible complications of these diseases include the following:

•     
Septicemia

•     
Osteomyelitis

•     
Meningitis

•     
Brain, liver, or splenic abscess

 

•     
presentation

•     
Generalized symptoms include fever, rigors, night sweats, myalgia,
anorexia, and headache. Additional symptoms, which are based on the route of
exposure, include chest pain, cough, photophobia, lacrimation, and diarrhea.

•     
There is nothing specific about the presentation of these diseases
and a strong clinical suspicion is required to assist in making a diagnosis in
endemic regions. This is particularly true for patients with predisposing
comorbidities, such as diabetes mellitus, chronic renal failure, alcoholism or
malignancy; those who are immunosuppressed as the result of either diseases or
drug treatment; and those living in or with a history of travel to endemic
areas. However, in the event of an intentional bacteriological attack in other
regions of the world, the above subsets of patients will be the most affected

•     
Generalized symptoms include fever, rigors, night sweats, myalgia,
anorexia, and headache. Additional symptoms, which are based on the route of
exposure, include chest pain, cough, photophobia, lacrimation, and diarrhea.

•     
There is nothing specific about the presentation of these diseases
and a strong clinical suspicion is required to assist in making a diagnosis in
endemic regions. This is particularly true for patients with predisposing
comorbidities, such as diabetes mellitus, chronic renal failure, alcoholism or
malignancy; those who are immunosuppressed as the result of either diseases or
drug treatment; and those living in or with a history of travel to endemic
areas. However, in the event of an intentional bacteriological attack in other
regions of the world, the above subsets of patients will be the most affected

Physical

Physical findings may include fever, cervical adenopathy,
hepatomegaly, or splenomegaly, and skin lesions including the following:.

Severe
urticaria has been reported during primary melioidosis
During
septicemia, flushing, cyanosis, and a disseminated pustular eruption can
be seen. Pustules often are associated with regional lymphadenitis,
cellulitis, or lymphangitis
Rarely,
ecthyma gangrenosum–like lesions and cutaneous abscesses (that sometimes
ulcerate) may develop

•     
DIAGNOSIS

Culture is the mainstay of
diagnosis. Ashdown’s agar

•      Microscopy  

Gram stain of sputum and abscess
pus may reveal gram-negative bacilli of B. pseudomallei

•      Serology  

 Serologic testing alone is
not a reliable method of diagnosis

Other tests include the following

Agglutination tests: Agglutination test
results may be positive after 7-10 days, but a high background titer found
in normal sera makes interpretation difficult.
Indirect hemagglutination tests
Polymerase chain reaction assays
Immunofluorescence assays
Enzyme immunoassays
Complement fixation tests

Complement fixation tests are more specific and are considered
positive for glanders if the titer is 1:20 or greater. A 4-fold increase in the
titer for melioidosis is considered positive.

•      The CBC may reveal a mild
leukocytosis with a left shift or leukopenia.

 

•      In melioidosis specifically,
laboratory studies may demonstrate anemia, leukocytosis, hepatic impairment,
renal insufficiency, and coagulopathy

 

Imaging Studies

Chest radiography may demonstrate bilateral bronchopneumonia,
miliary nodules, segmental or lobar infiltrates, and cavitating lesions. With
melioidosis, an abnormal chest radiography finding is present in up to 80% of
patients (usually diffuse nodular shadowing).

Ultrasonography and computed tomography may reveal multiple, small
discrete abscesses in both the liver and the spleen. These findings are highly
suggestive of visceral melioidosis.

Bone and soft tissue musculoskeletal involvement may be seen with
plain radiographs and magnetic resonance imaging. These findings are consistent
with disseminated melioidosis.

•      Management

•     
?  Implement barrier
protection with secretion precautions. While person-to-person transmission is
unlikely, isolation rooms for these patients are advisable. Patients should be
masked to prevent droplet dissemination.

•     
?  Obtain radiography, and
collect blood, urine, sputum, and skin lesion fluid.

•     
?  Initiate rapid administration
of supportive care and intravenous antibiotic therapy for severe disease.

•     
For local disease with mild toxicity, combine two of the three
regimens for 30 days, then switch to monotherapy with amoxicillin/clavulanate
or TMP-SMX for 60-150 days.

•     
For extrapulmonary suppurative disease, prolong treatment for 6-12
months. Drain abscesses surgically. For severe and/or septicemic disease,
initiate parenteral therapy for 2 weeks followed by oral therapy for 6 months
(ceftazidime combined with TMP/SMX 8 mg TMP/kg/d and 40 mg SMX/kg/d divided
qid). Add streptomycin when initiating treatment if plague
cannot be excluded.

•     
Alternative choices in severe cases of melioidosis include
imipenem-cilastatin or meropenem with or without trimethoprim/sulfamethoxazole.
Administration of these drugs may continue for up to 4 weeks, depending on
clinical response. Then, a 20-week course of doxycycline and TMP/SMX, which is
said to minimize the likelihood of relapse better than amoxicillin/clavulanate,
is administered.

•     
The prevention of relapse in melioidosis is critical since it has
been reported to occur in 23% of cases. Hence, the rationale behind the
prolonged therapy. Other antibiotics with activity against Burkholderia
pseudomallei include ceftriaxone, ticarcillin-sulbactam, and
aztreonam.

•     
Currently, no proven preexposure or postexposure prophylaxis is
available. Postexposure prophylaxis with TMP/SMX may be attempted. No vaccine
is available for human glanders or melioidosis

For acute human melioidosis, the most commonly recommended
treatment regimen consists of ceftazidime or a carbapenem followed by TMP/SMX.
For moderate to severe melioidosis, a treatment protocol from the Royal Darwin
Hospital in Australia consists of the following:

Ceftazidime 2 g IV q6h (50 mg/kg up to 1 g
in children) or
Meropenem 1 g IV q8h (25 mg/kg up to 1 g
in children) plus
Cotrimoxazole 320/1600 mg PO/IV BID (8/40
mg/kg up to 320/1600 mg in children).

This regimen is given for at least 14 days, but may have to be
continued for longer. Once the acute episode is resolved, then the eradication
period would commence.

•     
 

•