The patient developed fever and hypotension shortly after receiving blood products for variceal bleeding. This presentation is most consistent with transfusion-related acute lung injury (TRALI), which typically occurs within 6 hours of transfusion and involves rapid onset hypoxemia, hypotension, and bilateral pulmonary infiltrates due to an inflammatory reaction in the lungs.

1. Sepsis Mimics
Ashit V Hegde

2. Systemic Inflammatory Response Syndrome
(SIRS)
Core temperature >38 C or <36 C
Elevated heart rate (>90 beats/min)
Respiratory rate >20 breaths/min
 or PaCO2 <32 mm Hg
 or mechanical ventilation
WBC count >12,000 cells/mm3
 or <4,000 cells/mm3
 >10% immature cells

3. Traditional Mimics
• Burns
• Pancreatitis
• Trauma
• Pulmonary Embolism
• Myocardial Infarction
• Gi Hemorrhage
• Drug Reaction

4. The Real Sepsis Mimics
Present usually with Multi Organ Dysfunction
Occasionally Fever & Hypotension

5. CASE I
• 48 year male on treatment for NHL.
• Was admitted with severe fatigue, fever, diarrhea and new onset confusion.
• He was hypotensive and had decreased oxygen saturation on presentation in
ER.
• Clinical examination revealed a skin rash with tiny, clear, non-pruritic pustules
on bilateral upper extremities, hepato-splenomegaly (on ultrasound).
• CBC revealed Hb 8.1 g/dL, WBC 2900 (N55 L 35 M 10), platelets 95000.
• Peripheral smear : Thrombocytopaenia, no Malarial parasites
• Bilirubin 1.5 mg/dL, ALT 156 IU/L, and AST 473 IU/L,
• Fibrinogen 117 mg/dL, PT 12.3 s, PTT 38.0 s),
• D-dimer 0.92 μg/mL (0.00–0.40), LDH 4108 IU/L,
• What is the likely diagnosis

6. What is the likely diagnosis
•1) Dengue
•2) Neutropaenic Sepsis
•3) TTP
•4) Secondary HLH

7. Classification of HLH
• Consensus statement by the Histiocyte Society steering committee
published in 2018 .
• HLH is classified under 3 categories:
• Primary “familial” HLH, when there is a family member affected by
HLH or a known genetic defect in lymphocyte cytotoxicity
• MAS (macrophage activation syndrome)-HLH,3 where there is an
underlying auto- immune condition triggering the pathologic
inflammation
• Secondary HLH, often associated with underlying medical
conditions such as infections (eg, Epstein-Barr virus ),
malignancy (mostly lymphoid), metabolic disorders, or inherited
or secondary immunodeficiencies

9. MAS in Adults:
HS Score
Contains nine variables.
Score ranges from 0 to 317
Values >169 provide the best
cut-off.
Sensitivity 93% ,Specificity 86%
Allowing correct classification of
90% of cases

10. An inability of the
immune system to
adequately restrict
stimulatory effects
of various triggers.

14. Case II
• Day 0 : 57 year old male admitted with NSTEMI
• Treated with antiplatelets and LMWH
• Day 1 : develops fever and delirium
• CBC reveals Thrombocytopaenia, WBC count and Hb - OK
• LMWH and Clopidrogel temporarily withheld
• Day 2 : Continues to have fever (On Meropenem)
• Thrombocytopaenia worsening , worsening renal function
• Becomes deeply unconscious and needs intubation
• MRI reveals extensive bilateral tiny infarcts with hemorrhagic
transformation in some
• 2 D ECHO no clot

15. What is the likely diagnosis

16. Catastrophic APLA syndrome (CAPS)
• A very severe variant of the classic APS.
• Characterised by multiple organ involvement developing
over a very short period of time.
• Histopathological evidence of multiple small vessel
occlusions
• Presence of anti- phospholipid antibodies (aPL), usually in
high titre

17. CAPS – Clinical Manifestations
• The most common trigger for CAPS is infection.
• Other less common causes are :
• Anticoagulation withdrawal or low (INR),
• Medications (e.g., oral contraceptive),
• Obstetric complications,
• Neoplasia,
• SLE flares,
• Trauma and surgery.
• In almost 50%, no obvious precipitating factors
• CAPS can occur in patients without previous thrombotic

18. CAPS – Clinical Manifestations
• Single venous or arterial occlusions are uncommon.
• Thrombotic microangiopathy involving multiple organs is
responsible for the majority of the clinical features;
• Patients may present with pre- dominantly single organ
involvement, but they rapidly develop multiple organ
thrombosis leading to organ failure.
•

24. CASE III
• 56 year diabetic suffered an attack of Gout 3 weeks ago.
• Was treated
• Now presents with high grade fever, rash , liver and renal
dysfunction
• Hb 12.5 gm/dl WBC 9600 (N 40 E 22 L 30 M 8) Platelets 125000
• SGOT 560 SGPT 520 Bilirubin 2.8

25. The DRESS syndrome

26. The DRESS syndrome
• Incidence of organ involvement in DRESS syndrome
• Liver 80%
• Kidney 40%
• Pulmonary 33%
• Cardiac/muscular 15%
• Pancreas 5%
• Incidence of hematologic abnormalities in DRESS syndrome
• Atypical lymphocyte 63%
• Eosinophilia 52%
• Lymphocytopenia 45%
• Thrombocytopenia 25%
• Lymphocytosis 25%

28. Case IV
• 54 year patient with CLD no other co morbidities
• Admitted with variceal bleeding, undergoes banding
• Receives 4 Units of FFP
• Develops Fever , hypotension and Hypoxia 4 hours later
• What is the most likely cause

29. TRALI
• The clinical manifestations of TRALI usually occur within six
hours of transfusion.
• The common clinical presentation consists of rapid onset of
severe hypoxia, marked systemic hypovolaemia and
hypotension.
• Fever and rigors may be present.
• Radiographic investigations usually reveal bilateral
interstitialpulmonary infiltrates typical of ARDS..

30. Adrenal Crisis
• Abdominal pain, nausea/vomiting,
• Diarrhea, weakness, fatigue, salt craving, and
hypotension resistant to IV fluids/vasopressors.
• - Evaluate carefully for risk factors such as corticosteroid
use over two weeks, cancer, and tuberculosis.
• - Laboratory findings often include hyponatremia,
hyperkalemia, hypoglycemia, Eosinophilia and
hypercalcemia

31. Thyroid storm
• tachycardia,
• altered mental status,
• tremors,
• fever,
• GI symptoms, and
• often elevated WBC counts.

32. Cytokine release syndrome
• CRS is apotentially life-threatening complication of modern
targeted treatment (immunotherapy/targeted therapy) of
malignancies, especially relapsed or refractory acute
lymphoblastic leukemias
• The incidence of CRS of variable severity ranges from 50%
(blinatumomab) to 100% (chimeric antigen receptor T-cells –
CAR-TC)
• The pathophysiological mechanism is treatment-induced
activation of T-lymphocytes with extensive release of
proinflammatory cytokines