Sciresol Sciresol https://www.jcbsonline.ac.in/ Journal of Clinical and Biomedical Sciences 2319-2453 10.58739/jcbs/v14i2.24.12 CASE REPORT Symmetric Peripheral Gangrene Secondary to Sepsis Symmetric peripheral gangrene Mani Mohan Reddy K P Manimohanhp@gmail.com 1 Srinivasa S V 2 Postgraduate, Department of General Medicine, Sri Devraj Urs Academy of Higher Education and Research Kolar, Karnataka India Professor & HOU, Department of General Medicine, Sri Devraj Urs Academy of Higher Education and Research Kolar, Karnataka India 14 2 56 2024 <bold id="s-703d1fffc279">Abstract</bold>

Symmetrical peripheral gangrene (SPG) is described as rapid onset of peripheral and symmetrical gangrene in the lack of large vessel occlusive disease with high mortality rate.1 Hereby reporting an event of Upper limb symmetrical gangrene caused by septic shock in MODS, Acute myocarditis and was managed by inotropes. The case shows Symmetrical peripheral gangrene as a complication of sepsis owing to systematic imbalance that disturbs the organ dysfunction mainly coagulation and microcirculation. Primary recognition and quick management of sepsis and weaning off the inotropes at the initial opportunity are essential to evade Symmetrical peripheral gangrene.

 Keywords Symmetric peripheral gangrene MODS Sepsis Myocarditis Inotropes None 1 <bold id="s-7fa752bade45">Introduction</bold>

SPG is a rare condition categorized by ischemic damage distally leading to symmetrical gangrene of digits with absence of large vessel vasculitis or obstruction. Disseminated intravascular coagulation (DIC) and hemorrhagic infarction of skin where proximal arteries are not involved as trademark in this condition. 2

2 Case Study

A 30yr elderly female, with no history of co morbidities came to EMD with complaints of fever and breathlessness. Clinical examination revealed pulse rate of 106 bpm, BP-110/70 mm Hg, saturation -86% at room atmosphere, RR-38cpm, febrile, normal random blood sugar levels, pallor present. Systemic examination of RS showed bilateral rhonchi were present and other systemic examination normal. Patient was intubated in EMD I/V/O tachypnea and respiratory distress type 1.

Physical examination

Only pallor present.

N/k/c/o smoker, alcohol.

2.1 <bold id="strong-2846e8032cd9439a879aa55824b8e3d3">Investigations</bold>

ECG Shows poor R wave progression.

SOB profile: CKMB:60.60g/ml, MYO:329 ng/ml, TROP-I:7.32ng/ml, BNP-222pg/ml, DDIM:3230ng/ml.

2d Echo-normal chamber dimensions, no RWMA, (LVEF-55%), adequate LV systolic function, thin IAS, mild MR, mild AR, mild PR, mild TR, no clot, no veg.

Malaria, leptospira, dengue: negative.

<bold id="s-512dbefb2e1d">Case parameters</bold>

HB (g/dl)

7.6

6.6

6.8

7.8

8.1

9.8

TC (per cumm)

5.54

9.14

17.55

13.7

15.37

7.51

PLT (lakh)

50

73

76

88

399

345

BU (mg/dl)

38

42

70

44

45

23

SC (mg/dl)

1

0.9

0.9

0.8

0.7

0.7

<bold id="strong-6f2423f3560343019058f1e512e8c7a0">L</bold> <bold id="strong-8023b13ff5194e489be3be0f74e74385">iver function test</bold>

TB

DB

SGOT

SGPT

ALP

ALB

A:G

TP

DAY 1

2.29

1.83

110

43

119

2.2

1.0

4.6

DAY 5

1.3

1.2

208

109

131

2.3

1.1

5.9

Chest X-Ray

Day 1: B/L diffuse non homogenous opacities left & right.

(B/l bronchopneumonia)

Day 3: B/L diffuse non homogenous opacities left<right.

Day 6: B/L diffuse non homogenous opacities left (resolved), right (present).

On 2nd day evening patient started with inotropes i/v/o hypotension. Repeat Chest X-ray suggestive of Bronchopneumonia and Inj. furosemide 5mg/hr was started. On day 3 patient developing bluish discoloration of digital tips of both upper limbs. Lipid profile was with in normal limits, we changed to higher antibiotics for raising total leukocyte counts.

<bold id="s-ca759fb08efb">Clinical parameters</bold>

HbA1C

S. Phosphorous

S. Calcium

S. Magnesium

5%

6.3mg/dl

10.6 mg/dl

1.5 mg/dl

On examination all pulses which are peripheral are palpable, c-reactive protein is positive, erythrocyte sedimentation ratio is 150mm/hr, PT 22.3sec (control 14sec) and INR 1.93 aPTT 31.6 sec (control 28 sec), urine routine showing traces proteins and 1-2 pus cells in urine, S.LDH-843.

<bold id="strong-5875e25ba62a4ab09c8190fe27acaa09"/> <bold id="strong-1dc7785e1aed4e82be3481af80d5fb19">Day 1: B/L diffuse NHO on left</bold> <bold id="strong-24376bb7264b4aeb9282678a4f2f9ab4"> </bold> <bold id="strong-bab8a1e8bc8b404bb28f6d7b185c1367">&</bold> <bold id="strong-c7e4888d3e1a4c19b18c39e6bd55ed2c"> </bold> <bold id="strong-be76406dd9454d4caccd0a1e00d91e21">right</bold> <bold id="strong-7147a120321f42f1b933ecb8094ebbb0">Day 3: B/L diffuse </bold><bold id="strong-adb119a8f763432c8bea98826d370aa5">NHO on left < right</bold> <bold id="strong-c7f1af13bda44f359b8aad4852ba37cc">Day 6: B/L diffuse non homogenous opacities left (resolved), right (present)</bold>

Further investigations

Ultrasound abdomen showing normal size kidneys and echotexture. Arterial color Doppler study of bilateral upper limb shows triphasic spectral flow with normal PSV. Subclavian artery could not be assessed due to uncooperative patient.

ANA screening done and anti-nuclear antibody levels 1.37 units (negative). Then we switched to meropenem antibiotic on day 2. LFT returned to normal, leukocyte count return to normal on day 10. Urine culture and blood culture sensitivity showing no growth after 48 hrs of incubation.

Patient was diagnosed as MODS (ARDS, Sepsis, Thrombocytopenia, Acute Liver Injury) and Bronchopneumonia. On the aggressive management, the patient recovered on day 6 and extubated and shifted to ward on hospital day 10.

<bold id="strong-2abf2ed3fa1e42369c8ea3409e091bd1">Image showing B/L symentrical gangrene of upper limb</bold> 3 <bold id="s-2f4176d51408">Discussion</bold>

The mechanism under this condition is unknown but some studies show endothelial damage which is associated with hypercoagulable condition leading to occlusion of micro-circulation. 3 The causes might be bacterial, parasitic, viral infection or other conditions like vasopressors usage, cardiogenic shock, paraneoplastic syndrome, pulmonary embolism, and malignancies.2 Aggravating factors like decreased immunity condition, Absent spleen, old cold injuries to digits, renal failure, diabetes mellitus, increased sympathetic tone and vasopressors usage. 4, 5

Most of the cases are caused by bacterial septicemia are leading to death and diseased. DIC is related to majority of cases and common mechanism is occlusion of micro- circulation. 6

We should suspect immediately when digits undergo coldness, cyanosis, pain, pallor in the extremities, as the disorder rapidly progressive to cyanosis in digits and gangrene. As ischemic changes start distally and progress to the whole limb. 1

These features are associated with intact distal pulses and sparing of large vessels which are ruled out by Doppler study. The commonly affected areas are distal extremities, Scalp, Tip of the nose and genitalia and having the condition of shock and hypotension. Lab investigations are focused on the underlying condition.

The amputated specimen under staining shows thrombi obstructing the small vessels and sparing the large vessels. The treatment should be focused on primary etiology.

There is no treatment which is effective. Recognition and early discontinuation of vasopressor therapy and active management towards the sepsis and DIC are the main mechanisms towards SPG management. 6

In extreme cases amputation of gangrenous area may be necessary to save life.

 4 <bold id="s-b9f1722fcfea">Conclusion</bold>

Symmetrical peripheral gangrene (SPG) is the condition where there is high case mortality and morbidity. We have to highly think about SPG and rapid management towards SPG to save the life and limb saving from gangrene. 7

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