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Varicella zoster infection and pulmonary complications
European Journal of Internal Medicine 16 (2005) 449 – 450 www.elsevier.com/locate/ejim
Brief report
Varicella zoster infection and pulmonary complications Eyal Dahan, Claudia Simsolo, Monir Merei, Fina Vigder, Imad Tatoor, Arnon Blum * Department of Internal Medicine A, and the Imaging Department, Poria Medical Center, Lower Galilee 15208, Israel Received 11 October 2004; received in revised form 24 January 2005; accepted 3 February 2005
Abstract A 34-year-old immunocompetent man with varicella zoster (VZ) infection developed deep vein thrombosis and pulmonary embolism after suffering severe pneumonitis. He recovered after treatment with acyclovir, high-dose steroids, and ventilatory support. The endothelial damage could be a direct link between VZ pneumonitis and pulmonary emboli. D 2005 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. Keywords: Varizella zoster; Pulmonary emboli; Deep vein thrombosis
1. Introduction Only 2% of chickenpox infections [varicella zoster (VZ) virus] occur in adults; however, 25% of the fatalities caused by VZ occur in this age group [1]. Systemic complications include encephalitis, bacterial infections, sepsis, thrombocytopenia, thromboembolism, keratitis, conjunctivitis, uveitis, nephritis, the syndrome of inappropriate ADH secretion (SIADH), myocarditis, orchitis, and Henoch – Schonlein purpura. Involvement of the liver, spleen, pancreas, lymph nodes, and esophagus has been documented in postmortem studies [2]. We describe a young man who developed VZ pneumonitis and later deep vein thrombosis (DVT) and massive pulmonary emboli (PE). We suggest that there may be a direct pathophysiological link between VZ pneumonitis and venous thromboembolism in this case.
2. Case report A 34-year-old heavy smoking (20 pack/years) male was admitted to the hospital because of epigastric pain, nausea, and fever that had started 2 days earlier. On the day of
* Corresponding author. Tel./fax: +972 4 6652687. E-mail address: [email protected] (A. Blum).
admission, a varicelliform rash appeared all over his body in different stages of development. His son had recently been infected with chickenpox and, as far as he remembered, he had not been infected with chickenpox before. He denied coughing, having shortness of breath, or chest pain. The patient was obese (120 kg), but without signs of respiratory distress. He had a fever of 38.7 -C, a regular pulse (100 beats/ min), and a respiratory rate of 14 breaths/min. A diffuse, vesicular, maculo-papular rash in different stages of development covered the trunk, face, and extremities. Erythema covered the pharynx but without infiltration. Heart sounds were clear without murmurs or pathological sounds. The lungs were normal to auscultation and percussion. Lymph node enlargement up to 1 cm was documented in the neck and the groin. There were stasis dermatitis and varicose veins on both legs with no signs of DVT. The patient stayed in our ward from admission until discharge in an isolated room. He was not immunocompromised and was negative for HIV. Laboratory studies were normal except for creatinine phosphokinase (CPK) 437 U/L (normal: 30– 170), aspartate transaminase (AST) 230 U/L (normal: 5 –40), alanine transaminase (ALT) 227 U/L (normal: 1 –37), and lactic dehydrogenase (LDH) 1649 U/L (normal: 313 –618). Chest X-ray, electrocardiogram, and abdominal ultrasound were normal. On the 3rd day, the patient reported shortness of breath and his arterial saturation fell to 86% without oxygen support. Arterial blood gases demonstrated a pH of 7.36, pCO2 40 mm Hg, pO2 59 mm Hg, and bicarbonate 22.6
0953-6205/$ - see front matter D 2005 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.ejim.2005.02.011
450
E. Dahan et al. / European Journal of Internal Medicine 16 (2005) 449 – 450
rash disappeared. All liver enzymes returned to normal. Another echocardiogram showed normal findings with normal right and left diameters and function without pulmonary hypertension. On discharge the patient was stable and feeling well. We recommended continuing warfarin treatment for the next 6 months to achieve an INR of 3.5 and to follow-up liver and lung function tests.
3. Discussion
Fig. 1. CT angiography, pulmonary artery protocol. Axial view caudal from the carina level shows a thrombus in the distal branches of pulmonary arteries.
mmol/L. Chest X-ray demonstrated diffuse reticulo-nodular infiltrates over both lungs. Oxygen and non-invasive ventilation (BiPAP) were initiated since the patient was dyspneic and had severe shortness of breath. Intravenous acyclovir 750 mg daily was started for 10 days with intravenous solumedrol 62.5 mg daily for 2 weeks; then the dose was tapered down gradually. The patient also started to complain of a dull abdominal pain, and a repeat abdominal ultrasound documented an enlarged spleen (15 cm). After starting with BiPAP, his breathing and shortness of breath improved. Two weeks later, we noticed swelling of the right leg, and a Doppler ultrasound confirmed the diagnosis of deep vein thrombosis (DVT) of the right popliteal and right saphenous veins as well as of the superficial right saphena magnum vein. Low molecular weight heparin (enoxaparin) was started (1.5 mg/kg o.d.). Three days later, the patient had severe respiratory deterioration with dyspnea, tachypnea, and a PO2 of 50 mm Hg. Spiral CT demonstrated thrombi in the large and segmental pulmonary arteries on both sides (Fig. 1). Enoxaparin dosage was increased (2 mg/kg o.d.) and warfarin was started. An echocardiogram demonstrated right ventricular enlargement of 45 mm with an elevated pulmonary pressure of 50 mm Hg with normal diameter and function of the left ventricle. We continued to treat him in the same way with gradual improvement. After 3 weeks he became less oxygendependent, arterial blood gases returned to normal, and the
It has already been suggested that herpes viruses may induce endothelial damage, atherosclerosis, and thromboembolism [3]. The varicella virus has specifically been associated with vascular damage in various organs including the lungs, pleura, and brain [4]. The vascular damage we saw may have been caused by a virus infecting endothelial cells [5]. Our patient showed involvement of several organs: the pharynx, lungs, right leg, spleen, liver, lymph nodes, heart, and possibly the brain. It is possible that disseminated endothelial injury is responsible for the widespread organ involvement that can occur in chickenpox. The incidence of pneumonitis after varicella infection in healthy adults varies from 5% to 50% [1]. Overall mortality is between 10% and 30%, but increases up to 50% among the severe cases that develop respiratory failure [1]. Pulmonary thromboembolism is a rare and serious complication of VZ infection. Epidemiological data regarding the incidence of thromboembolism in VZ infection are lacking, and most of the cases that have been reported have been in children [2]. Thromboembolic events could be secondary to transient protein-S deficiency, which has been documented after varicella infection, caused by antiprotein-S antibodies [2].
References [1] Feldman S. Varicella-zoster virus pneumonitis. Chest 1994; 106(1 Suppl):22S – 7S. [2] McColl MD, Chalmers EA, Rafferty I. Pulmonary embolism associated with varicella infection. Br J Haematol 1998;102(5):1384 – 5. [3] Minik CR, Fabricant CG, Fabricant J, Litrenta MM. Atherosclerosis induced by infection with herpes virus. Am J Pathol 1970;96:673 – 706. [4] Sargent EN, Carson MJ, Reilly ED. Roentgenographic manifestations of varicella pneumonia with post mortem correlations. Am J Roentgenol 1966;98:305 – 17. [5] Friedman HM, Macarak EJ, MacGregor RR, Wolf J, Kefalides NA. Virus infection of endothelial cells. J Infect Dis 1981;143:266 – 73.
Brief report
Varicella zoster infection and pulmonary complications Eyal Dahan, Claudia Simsolo, Monir Merei, Fina Vigder, Imad Tatoor, Arnon Blum * Department of Internal Medicine A, and the Imaging Department, Poria Medical Center, Lower Galilee 15208, Israel Received 11 October 2004; received in revised form 24 January 2005; accepted 3 February 2005
Abstract A 34-year-old immunocompetent man with varicella zoster (VZ) infection developed deep vein thrombosis and pulmonary embolism after suffering severe pneumonitis. He recovered after treatment with acyclovir, high-dose steroids, and ventilatory support. The endothelial damage could be a direct link between VZ pneumonitis and pulmonary emboli. D 2005 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. Keywords: Varizella zoster; Pulmonary emboli; Deep vein thrombosis
1. Introduction Only 2% of chickenpox infections [varicella zoster (VZ) virus] occur in adults; however, 25% of the fatalities caused by VZ occur in this age group [1]. Systemic complications include encephalitis, bacterial infections, sepsis, thrombocytopenia, thromboembolism, keratitis, conjunctivitis, uveitis, nephritis, the syndrome of inappropriate ADH secretion (SIADH), myocarditis, orchitis, and Henoch – Schonlein purpura. Involvement of the liver, spleen, pancreas, lymph nodes, and esophagus has been documented in postmortem studies [2]. We describe a young man who developed VZ pneumonitis and later deep vein thrombosis (DVT) and massive pulmonary emboli (PE). We suggest that there may be a direct pathophysiological link between VZ pneumonitis and venous thromboembolism in this case.
2. Case report A 34-year-old heavy smoking (20 pack/years) male was admitted to the hospital because of epigastric pain, nausea, and fever that had started 2 days earlier. On the day of
* Corresponding author. Tel./fax: +972 4 6652687. E-mail address: [email protected] (A. Blum).
admission, a varicelliform rash appeared all over his body in different stages of development. His son had recently been infected with chickenpox and, as far as he remembered, he had not been infected with chickenpox before. He denied coughing, having shortness of breath, or chest pain. The patient was obese (120 kg), but without signs of respiratory distress. He had a fever of 38.7 -C, a regular pulse (100 beats/ min), and a respiratory rate of 14 breaths/min. A diffuse, vesicular, maculo-papular rash in different stages of development covered the trunk, face, and extremities. Erythema covered the pharynx but without infiltration. Heart sounds were clear without murmurs or pathological sounds. The lungs were normal to auscultation and percussion. Lymph node enlargement up to 1 cm was documented in the neck and the groin. There were stasis dermatitis and varicose veins on both legs with no signs of DVT. The patient stayed in our ward from admission until discharge in an isolated room. He was not immunocompromised and was negative for HIV. Laboratory studies were normal except for creatinine phosphokinase (CPK) 437 U/L (normal: 30– 170), aspartate transaminase (AST) 230 U/L (normal: 5 –40), alanine transaminase (ALT) 227 U/L (normal: 1 –37), and lactic dehydrogenase (LDH) 1649 U/L (normal: 313 –618). Chest X-ray, electrocardiogram, and abdominal ultrasound were normal. On the 3rd day, the patient reported shortness of breath and his arterial saturation fell to 86% without oxygen support. Arterial blood gases demonstrated a pH of 7.36, pCO2 40 mm Hg, pO2 59 mm Hg, and bicarbonate 22.6
0953-6205/$ - see front matter D 2005 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.ejim.2005.02.011
450
E. Dahan et al. / European Journal of Internal Medicine 16 (2005) 449 – 450
rash disappeared. All liver enzymes returned to normal. Another echocardiogram showed normal findings with normal right and left diameters and function without pulmonary hypertension. On discharge the patient was stable and feeling well. We recommended continuing warfarin treatment for the next 6 months to achieve an INR of 3.5 and to follow-up liver and lung function tests.
3. Discussion
Fig. 1. CT angiography, pulmonary artery protocol. Axial view caudal from the carina level shows a thrombus in the distal branches of pulmonary arteries.
mmol/L. Chest X-ray demonstrated diffuse reticulo-nodular infiltrates over both lungs. Oxygen and non-invasive ventilation (BiPAP) were initiated since the patient was dyspneic and had severe shortness of breath. Intravenous acyclovir 750 mg daily was started for 10 days with intravenous solumedrol 62.5 mg daily for 2 weeks; then the dose was tapered down gradually. The patient also started to complain of a dull abdominal pain, and a repeat abdominal ultrasound documented an enlarged spleen (15 cm). After starting with BiPAP, his breathing and shortness of breath improved. Two weeks later, we noticed swelling of the right leg, and a Doppler ultrasound confirmed the diagnosis of deep vein thrombosis (DVT) of the right popliteal and right saphenous veins as well as of the superficial right saphena magnum vein. Low molecular weight heparin (enoxaparin) was started (1.5 mg/kg o.d.). Three days later, the patient had severe respiratory deterioration with dyspnea, tachypnea, and a PO2 of 50 mm Hg. Spiral CT demonstrated thrombi in the large and segmental pulmonary arteries on both sides (Fig. 1). Enoxaparin dosage was increased (2 mg/kg o.d.) and warfarin was started. An echocardiogram demonstrated right ventricular enlargement of 45 mm with an elevated pulmonary pressure of 50 mm Hg with normal diameter and function of the left ventricle. We continued to treat him in the same way with gradual improvement. After 3 weeks he became less oxygendependent, arterial blood gases returned to normal, and the
It has already been suggested that herpes viruses may induce endothelial damage, atherosclerosis, and thromboembolism [3]. The varicella virus has specifically been associated with vascular damage in various organs including the lungs, pleura, and brain [4]. The vascular damage we saw may have been caused by a virus infecting endothelial cells [5]. Our patient showed involvement of several organs: the pharynx, lungs, right leg, spleen, liver, lymph nodes, heart, and possibly the brain. It is possible that disseminated endothelial injury is responsible for the widespread organ involvement that can occur in chickenpox. The incidence of pneumonitis after varicella infection in healthy adults varies from 5% to 50% [1]. Overall mortality is between 10% and 30%, but increases up to 50% among the severe cases that develop respiratory failure [1]. Pulmonary thromboembolism is a rare and serious complication of VZ infection. Epidemiological data regarding the incidence of thromboembolism in VZ infection are lacking, and most of the cases that have been reported have been in children [2]. Thromboembolic events could be secondary to transient protein-S deficiency, which has been documented after varicella infection, caused by antiprotein-S antibodies [2].
References [1] Feldman S. Varicella-zoster virus pneumonitis. Chest 1994; 106(1 Suppl):22S – 7S. [2] McColl MD, Chalmers EA, Rafferty I. Pulmonary embolism associated with varicella infection. Br J Haematol 1998;102(5):1384 – 5. [3] Minik CR, Fabricant CG, Fabricant J, Litrenta MM. Atherosclerosis induced by infection with herpes virus. Am J Pathol 1970;96:673 – 706. [4] Sargent EN, Carson MJ, Reilly ED. Roentgenographic manifestations of varicella pneumonia with post mortem correlations. Am J Roentgenol 1966;98:305 – 17. [5] Friedman HM, Macarak EJ, MacGregor RR, Wolf J, Kefalides NA. Virus infection of endothelial cells. J Infect Dis 1981;143:266 – 73.