Subcutaneous fat necrosis (SCFN) secondary to therapeutic hypothermia with persistent leucocytosis in a neonate

2021 ◽  
Vol 6 (2) ◽  
pp. 01-04
Author(s):  
Sandhya Govindarajan

We report a term male neonate, born to consanguineous parents through a difficult labour who needed resuscitation at birth, followed by ventilation for respiratory distress. In view of suspected Hypoxic Ischemic Injury, he was started on whole body cooling for 72 hours. He was treated as suspected sepsis with 5 days of intravenous antibiotics. On day 6, he was noted to have hard, painless skin nodules of his back and left arm which was clinically diagnosed as subcutaneous fat necrosis. His serum calcium and phosphate levels remained normal throughout hospital stay. His full blood counts and bone profile were monitored regularly. During follow-up at 6 weeks, his white cell counts continued to be high with 69% lymphocytes. To our knowledge, this is the first case of SCFN of a neonate associated with persistent leucocytosis. Haematological and metabolic complications should be closely monitored in a neonate with subcutaneous fat necrosis.

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Erhan Calisici ◽  
Mehmet Yekta Oncel ◽  
Halil Degirmencioglu ◽  
Gonca Sandal ◽  
Fuat Emre Canpolat ◽  
...  

Subcutaneous fat necrosis (SCFN) is an inflammatory disorder of adipose tissue. The main risk factors for the development of SCFN are perinatal asphyxia and hypothermia. Presented here is a case of a newborn who developed SCFN in association with polycythemia and hypocalcemia following treatment by passive cooling. Neonates who undergo passive or whole body cooling therapy should be closely monitored for any signs of SCFN.


2010 ◽  
Vol 146 (8) ◽  
Author(s):  
Vikash Oza ◽  
James Treat ◽  
Noah Cook ◽  
Michael T. Tetzlaff ◽  
Albert Yan

2019 ◽  
Vol 47 (9) ◽  
pp. 986-990 ◽  
Author(s):  
Mahdi Alsaleem ◽  
Lina Saadeh ◽  
Valerie Elberson ◽  
Vasantha H.S. Kumar

Abstract Objective To describe the clinical characteristics and risk factors in infants with subcutaneous fat necrosis (SFN) following therapeutic hypothermia for hypoxic-ischemic encephalopathy (HIE). Methods A case-control study was performed by a retrospective chart review of infants with moderate or severe HIE admitted to a level IV regional perinatal center and who underwent whole-body cooling. Results A total of 14 (8.1%) of 171 infants with moderate or severe HIE who underwent whole-body cooling developed SFN during hospitalization. There were more females [71% (10/14)] and large-for-gestational age (LGA) infants [28% (4/14)] in the SFN group vs. 36% females (57/157) and 8% LGA infants (13/157) in the group without SFN (P-values of 0.009 and 0.015, respectively). The mean lowest platelet count was lower 108 ± 55 109/L vs. 146 ± 62 109/L and the mean highest calcium level was higher 11.3 ± 2.5 vs. 10.6 ± 0.8 mg/dL in infants with SFN vs. infants without SFN, respectively (P-values of 0.0078 and 0.006, respectively). Distribution of skin lesions followed distinctive patterns representing the areas with direct contact with the cooling blanket. One infant developed severe, life-threatening hypercalcemia that required aggressive management, including diuretics, corticosteroids and bisphosphonates. Conclusion Although SFN is a rare complication of therapeutic hypothermia, it can be a life-threatening condition if complicated by severe hypercalcemia. Infants who undergo therapeutic hypothermia for HIE need regular skin examinations to evaluate for SFN. If SFN is identified, monitoring of serum calcium levels to prevent life-threatening hypercalcemia is recommended.


2019 ◽  
Vol 38 (4) ◽  
pp. 236-241 ◽  
Author(s):  
Mary Whalen

Subcutaneous fat necrosis (SCFN) is a rare complication, usually occurring in otherwise healthy full-term infants who have experienced some level of trauma that causes ischemic injury to adipose tissue. Tissue injury usually occurs in areas of the body that are exposed to excessive pressure as during delivery. Tissue injury has also been described secondary to therapeutic cooling. This case study presents an infant who received whole body cooling for hypoxic ischemic injury and later developed severe hypercalcemia at one month of age without the skin lesions consistent with SCFN. The differential diagnosis for hypercalcemia and how it relates to SCFN is presented, as well as clinical presentation, treatment, and prognosis.


2017 ◽  
Vol 21 (5) ◽  
pp. 502-506
Author(s):  
Salwa Khedr ◽  
Anna Piskorski ◽  
Adrienne R Bingham ◽  
Justin Goldstein ◽  
Abbot R Laptook ◽  
...  

Therapeutic hypothermia (head or whole-body cooling) improves survival and neurodevelopmental outcome in term newborns with moderate-to-severe encephalopathy. Hypothermia treatment is well tolerated; the most common side effect is thrombocytopenia. In about 1% of infants, focal subcutaneous fat necrosis has been reported. We describe a case of clinically unsuspected massive visceral fat necrosis in a term infant with Apgar score 0 at 1 min (“resuscitated apparently stillborn” infant) who was treated with therapeutic hypothermia for 72 h and expired on the 25th day of life following a neonatal course complicated by severe encephalopathy, pulmonary artery hypertension, persistent thrombocytopenia, hypoglycemia, and severe basal ganglia-thalamic abnormalities on magnetic resonance imaging. Postmortem examination revealed extensive visceral (brown) fat necrosis, involving thoracic, abdominal, and retroperitoneal adipose tissue, with distinctive sparing of the subcutaneous (white) fat. The fulminant—yet clinically occult—visceral fat necrosis seen in this case suggests that (lesser degrees of) fat necrosis may go unrecognized in hypoxic-ischemic newborns, especially in those treated with hypothermia, and underscores the importance of close monitoring of encephalopathic newborns both in the short and long terms for complications of fat necrosis (hypercalcemia and nephrocalcinosis).


1982 ◽  
Vol 48 (03) ◽  
pp. 245-246 ◽  
Author(s):  
V Hofmann ◽  
P G Frick

SummaryA female patient is described who developed skin and subcutaneous fat necrosis on two occasions after intake of acenocoumarol.Several months later identical skin changes occurred during an episode of cholestasis associated with a prolongation of the prothrombin time to an extent comparable with therapeutic anticoagulation; intake of oral anticoagulants could be excluded.This association gives new insights in the pathogenetic mechanisms responsible for the so-called coumarin necrosis and indicates that it may be not due to drug toxicity or allergy.


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