Case Presentation Febrile Neutropenia Nizar

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Case presentation:

Hemolytic Anaemia
NIZAR I.J, MBBS
INTERN OF INTERNAL MEDICINE
HMG OLAYA COMPLEX


Content

History of presenting illness

Physical examination

Investigations

Differential Diagnosis

Conclusion

Chief complaint

A 65 years old Diabetic Pakistani female,


complaining of fever, difficulty in breathing and
desaturation since 5 days before admission
History of presenting illness

Actually the condition started when the patient had an


episodes fever and shevering for 5 days, after coming from
Pakistan temperature was 39 - 40C

Then the patient complained of Shortness of Breath at


rest and was desaturated with respiratory distress

PAST MEDICAL HISTORY

Systemic Review:

- patient complained of drowsiness and dizziness

Decreased urine output, other Systems are all clear

Past Medical History:

- type II - DM on metformin and Sitagliptin

- No PMH of similar condition



Family History:

- No family history of similar condition

Positive family history of chronic diseases DM, HTN

Drug History:

- patient on metformin and sitagliptin

- patient is allergic to dry foods and nuts. And also allergic to some antibiotics
which was not specified by her

Social History:
- no bad habits, no home animals, have medical insurance

Physical examination
General look : looks ill, excessive sweating,
alert, slightly confused, not in distress now

Hands: regular pulse, no clubbing of fingers

Eyes: No pale or Jaundice

Mouth : No Central cyanosis

Neck: No LN enlargements

Chest Examination
Chest wall is symmetric. Without deformity

No tenderness is appreciated upon palpation of the chest


wall

The patient doesn't exhibit respiratory distress, but was


distressed in the ICU

Slight bibasal crackles

Resonance is normal upon percussion of all lung fields

Systemic examination

CVS: S1, S2 +0
Abdomen: Soft and lax, mild epigastric tenderness
CNS: conscious, oriented, intact motor and sensor across all
limbs, with right calf muscle swelling and hotness

Vital signs
TEMPERATURE: 38.3 C

PULSE RATE: 80/min


RESPIRATORY RATE: 20/min

BLOOD PRESSURE: 120/80


SPO2: 95%
WEIGHT: 70 kg

HIGHT: 152 cm

investigations

LABORATORY:

Total = 6.8
WBC
Neutrophils = 2.5 normal
Lymphocytes = 0.20
CRP 121

RBC = 3.8 low


CBC
HBG = 11 low

LDH 300 unit/ L

Bilirubin total 2 mg/dl


investigations

Cultures:

Stool : Occult blood, no ova or parasites

Malaria Smear - negative

Plan
Septic Workup

Perfalgan 1gm IV Q6H

Pantozol prophylactic 40mg IV once daily

Clexane prophylactic 60mg once daily

Insuline 4 Units SC Q4H

Lornoxicam (NSAID) 8 GM BID IV

Zyrtec 5 mg OD PO

Sulfa-metho-xazole (bactrime) 1 tab BID PO

Doxycycline 1 tab BID PO

Deferential diagnosis

Falciparum Malaria

Salmonella Typhoid

Brucellosis

Fungal infection

Abdominal TB

HIV

Hemolytic Anaemia

Hemolysis: is the premature breakdown of RBCS

It classified as: intravascular (occurs in the circulation) or


extravascular (in the reticuloendothelial system, ie macrophages of
liver, spleen, and bone marrow)

may be asymptomatic, but if the bone marrow does not compensate


sufficiently, a hemolytic anaemia results

How to Approach
to confirm hemolysis and then find the cause try to answer these
four questions:

1) is there increased red cell breakdown?

• Anaemia with normal or increased MCV.

• increased Bilirubin: unconjugated

• increased Urinary urobilinogen

• increased Serum LDH

How to Approach

2) Is there increased red cell production?

• increased Reticulocytes, causing increased MCV (reticulocytes


are large immature RBCS)

How to Approach
3) Is the hemolysis mainly extra- or intravascular?

Extravascular hemolysis = splenic hypertrophy and splenomegaly

intravascular hemolysis =

• free plasma hemoglobin: released from RBCS.

• Methaemalbuminaemia:

• Plasma haptoglobin: mops up free plasma Hb, then removed by the liver.

• Hemoglobinuria: causes red-brown urine, in absence of red blood cells.

• Haemosiderinuria

How to Approach

4) What is the cause of the hemolysis?


Work up
FBC, reticulocytes, bilirubin, LDH, haptoglobin, urinary urobilinogen. Thick and thin lms for malaria screen if
history of travel. The blood lm may show poly chromasia and macrocytosis due to reticulocytes, or point to the
diagnosis:

Further tests (if the cause is sti not obvious)

• Osmotic agility testing wi con rm the presence of membrane abnormalities which have been identi ed on the
lm.

• Hb electrophoresis wi detect haemoglobinopathies.

• The direct antiglobulin (Coombs) test

• Enzyme assays when other causes have been excluded.


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What are the causes

Acquired Hereditary

1. Immune-mediated/direct
antiglobulin test +ve Coombs test: 1. Enzyme defects: (G6PD, Pyruvate
(Drug-induced, Autoimmune kinase de ciency)
haemolytic anaemia) 2. Membrane defects: (Hereditary
2. Direct antiglobulin/Coombs Ωve spherocytosis, Hereditary
AIHA: (autoimmune hepatitis) elliptocytosis, Hereditary ovalocytosis
3. Microangiopathic haemolytic and stomatocytosis
anaemia (MAHA)
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What are the causes

Acquired Hereditary

4. Infection: Malaria
3. Hemoglobinopathy:
• Sickle-cell disease
5. Paroxysmal nocturnal
• Thalassaemia
hemoglobinuria
“ Give me problems, give me work, I crave for mental
exaltation, that’s why I have chosen my own particular
profession”

— Sherlock Holmes

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