Annals of Burns and Fire Disasters - vol. XII - n° 4 - December 1999

PERICARDIAL EFFUSION: A RARE COMPLICATION OF THERMAL BURN

Barr J., Sagi A., Glesinger R., Rosenberg L.

Department of Plastic Surgery, Assaf Harofeh Medical Centre, Tel-Aviv University, Sackler School of Medicine, Zerifin, Israel


SUMMARY. The heart is rarely affected by thermal injury, but here such a case is presented. Following severe burns a 28-yr-old woman suffered from pericardial effusion together with ARDS and sepsis. She had sustained 30% TBSA second- and third-degree burns in the face, neck, chest, arms, hands, abdomen, and thighs. Two days after admission the patient underwent tangential excision and skin grafting in the hand. The patient eventually developed ARDS, and in the second week post-burn her blood cultures were positive for Acinetobacter and enterococei. The patient was treated with intravenous imipenem, which according to sensitivity was later replaced by ampicillin and Garamycin. It was decided not to drain the pericardium but rather to continue conservative treatment with aspirin, antibiotics, and respiratory support. The patient's condition gradually improved and two months after admission she was discharged with all wounds closed. At follow-up several months later, she was free of respiratory complaints.

Introduction

Sepsis in the early period following a major burn is a very common and almost inevitable complication. Losing the protective skin barrier and immunological defence mechanisms opens the gate for bacteria to enter the blood stream and infect various organs and systems in the body.
The heart is among the less frequently injured organs following a thermal injury (2.1%).' We present the case of a woman who developed a post-burn pericardial effusion and several other complications, including ARDS and sepsis.

Case history

A young woman aged 28 yr tried to adjust the flame of the petroleum heater in her apartment. While she was doing so, her dress caught fire. An hour passed before she was found. She was brought to the emergency room with 30% T13SA second- and third-degree burns in the face, neck, chest, arms, hands, abdomen, and thighs.
Since the accident took place in a closed space, smoke inhalation was also suspected. There were signs of charing around the ala nasi. She was highly excited on admission, pale, and tachypnoeic (40 breaths per min), with shallow breathing and shivering. The vital signs were stable: blood pressure, 140/90; pulse, 11 0/min; respiration 35/min. The blood count showed a haemoglobin level of 9. Blood gases and electrolytes were within normal levels. There was no sign of burn or oedema in the nasopharynx. Chest x-ray and electrocardiogram were normal. After nasotracheal intubation, mechanical ventilation was started. A nasogastric tube was inserted and intravenous Tagamet 200 mg x 5/day was initiated. Intravenous fluid administration with Ringer's lactate solution (4 cc/kg/h) was also initiated. The burn wounds were cleaned and covered with saline dressing. The patient was then transferred to the intensive respiratory care unit (IRCU) for continuation of treatment and monitoring. During the following days she developed ARDS and mechanical ventilation was therefore continued. Two days after admission the patient underwent tangential excision and skin grafting in the hand.
In the second week blood cultures were positive for Acinetobacter and enterococci. Intravenous imipenem 3 gr/d was initiated, which according to sensitivity was later replaced by ampicillin 12 gr/d and Garamycin 80 mg x 3/d. The patient also gradually developed respiratory distress. The blood gases deteriorated and a chest x-ray revealed disseminated pulmonary infiltrates and cardiomegaly. Central venous pressure levels rose to nearly 30 cin H20 and a paradoxical pulse appeared. The fluid balance was 10 litres positive, and the patient was oliguric and needed furosemide intravenously a few times to maintain adequate urine output. The clinical picture was compatible with tamponade and the next step was to perform echocardiography. A large amount of pericardial fluid and a mild collapse of the left atrial walls were found. After a joint consultation with the cardiologists, the IRCU, and plastic surgeons, it was decided not to drain the pericardium but rather to continue conservative treatment with aspirin 2 gr/d, antibiotic treatment, and respiratory support. A slow but continuous improvement followed in the next few days. Central venous pressure levels dropped gradually, urine output increased, blood gases improved, and the respiratory distress subsided. Mechanical ventilation was terminated and the patient received a high calorie diet and vigorous physiotherapy. Repeated echocardiography showed only a residual amount of pericardial fluid. A second skin grafting operation was performed and two months after admission the patient was discharged with all wounds closed. At follow-up several months later, she was free of respiratory complaints.

Discussion

The systemic response to a major thermal burn injury is characterized by a rapid and massive loss of fluids. The loss of capillary integrity leads to the shift of fluids and plasma proteins from the vascular bed into the interstitial compartment.' Hypovolaernic shock results. The cardiovascular response exhibits an ebb-and-flow pattern. The ebb phase represents a 1-3 day period of decrease in cardiac output, which is mainly the reflection of hypovolaemic shock.' The following flow phase represents the highly increased metabolic demand, which lasts for several weeks and is characterized by a marked increase in cardiac output and peripheral blood flow. Cardiovascular complications become prominent when the partial- to full-thickness burn area exceeds 20-25% TBSA.' These complications are mainly attributed to infection and a decrease in body defence mechanisms.
In a large series of 3640 burn patients reviewed by Munster et al., 64 cases of infection involving the heart were identified.' There were only three survivors among them, equivalent to a mortality of 95.3%. The injured sites involved the myocardium in 34 patients, the valves in 18, multiple sites in 7, the pericardium in 4, and coronary artery in one. Pericarditis occurred in three patients owing to extension of myocardial infection through the epicardium, and in one patient resulted from mediastinitis secondary to infection spreading from a tracheotomy site. The pathogens responsible for the infection reflected the predominant organisms in the infected burn wound or cannulated vein. A diagnosis of purulent pericarditis should be suspected with the development of a heart murmur, cardiomegaly, pericardial friction rub, high fever with chills, night sweats, acute heart failure, hypotension, tachycardia, and elevation of central venous pressure.',' In the case we present here, the elevation of central venous pressure, cardiomegaly, the development of tachypnoea, the appearance of disseminated pulmonary infiltrates, a positive fluid balance of nearly 10 litres, and acute heart failure led us to hypothesize three possible causes: 1. superhydration-induced heart failure; 2. respiratory failure due to ARDS and septicaemia; 3. heart failure as a result of pericardial effusion, in view of the high central venous pressure levels. The subsequent echocardiography showed that indeed there was pericardial involvement. The decision not to drain the pericardium was based on the assumption that bacteria from the infected burned chest surface might contaminate the otherwise uninfected reactive pericardial effusion and complicate the patient's condition. Conservative treatment with antibiotics, aspirin, and respiratory support proved to be beneficial. Our conclusion is that conservative treatment should be considered in thermally injured patients complicated by pericardial effusion before pericardial drainage is carried out.

 

RESUME. Les Auteurs décrivent un cas peu commun où le coeur a été atteint par une lésion thermique. A la suite de brûlures graves une femme âgée de 28 ans souffrait d'effusion péricardiaque associée au SDRA et à la sepsis. Elle présentait des brûlures de 2ème et 3ème degré en 30% de la surface corporelle totale dans le visage, le cou, le thorax, les bras, l'abdomen et les cuisses. Deux jours après l'hospitalisation la patiente a subi l'excision tangentielle et la greffe cutanée à la main. La patiente à la fin présentait le SRDA, et dans la deuxième semaine après la brûlure les cultures du sang étaient positives pour l'Acinetobacter et les entérocoques. La patiente a été traitée avec l'imipenern intraveineux que selon la sensibilité a été remplacé par l'ampicilline et le Garamycin. Il a été décidé de ne pas drainer le péricarde et de continuer plutôt le traitement conservateur avec l'aspirine, les antibiotiques et le support respiratoire. Les conditions de la patiente ont amélioré graduellement et deux mois après l'hospitalisation elle a été renvoyée guérie quand toutes les lésions étaient guéries. Le contrôle effectué après divers mois a montré qu'elle ne souffrait plus de problèmes respiratoires.


BIBLIOGRAPHY

  1. Munster A.M. et al.: Cardiac infections in burns. American J. Surgery, 122: 524-7, 1971.
  2. Carleton S.C. et al.: Cardiac problems associated with burns. Cardiology Clinics, 13: 257-60, 1995.
  3. Nakamura K. et a].: Survival of an extensively burned infant following purulent pericarditis. Burns, 11: 202-6, 1985.
  4. Srivastava R.K. et al.: Cardiac infection in acute burn patients. Burns, 6: 48-54.

 

This paper was received on 18 October 1999.

Address correspondence to:

Dr Jacob Barr
8 Yassour St., POB 2292, Lehavim 85338, Israel
Tel.: 972-7-6512628; fax: 972-7-6519076/8; mobile: 972-50-214850
E-mail: gbarr@isdn.net.il



 

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