- Email: [email protected]
COMPLICATION OF CENTRAL VENOUS CATHETERISATION
1092
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She also had a cytomegalothen considered and she was given oral steroids, intravenous teniposide, and intrathecal methotrexate.4 Within a week there was a considerable clinical and laboratory improvement. Foscarnet infusions were given during the second and third week of chemotherapy as a protection against generalised CMV infection. The antiviral therapy did not seem to contribute to the continuous recovery already seen in the first week of chemotherapy. If the girl had instead been classified as VAHS, cytotoxic therapy, which we think was life-saving, would not have been considered. Some of the patients classified as VAHS by Risdall et al,l especially those lacking apparent underlying disease, may have had HLH, although it is difficult to judge because, for example, analyses of lipids and CSF were not presented. Some of the patients receiving azathioprine and prednisone, mainly the renal transplant recipients who had undergone splenectomy, may have had a benign reactive state of histiocytic proliferation with some erythrophagocytosis. This is underlined by the fact that in the latter group only 5 out of 14 patients had hepatomegaly, whereas Janka found hepatomegaly in 94% of the patients with HLH.5 The immunocompromised condition of these patients might have contributed to the aggressive picture in this otherwise harmless reaction. Thus we hesitate to use the diagnosis VAHS, although we admit that the massive histiocytic proliferation in immunocompromised patients is interesting and needs further evaluation. We suggest that the proposed classification of histiocytosis syndromes in children be changed so that HLH and VAHS are considered as the same disease and classified as HLH. The commonly used term "familial", in familial erythrophagocytic lymphohistiocytosis, may be misleading, and we think that haemophagocytic lymphohistiocytosis is a better name for this disease.
hyperplasia with erythrophagocytosis.
subclavian vein, and the catheter tip lay parallel to the walls of the
virus
SVC on the control chest X-ray. Two days later she was dyspnoeic. On the third day she suddenly became- hypotensive and acutely dyspnoeic. She was transferred to an intensive care unit: she was pale and cyanotic, systolic blood pressure was 60-80 mm Hg and .pa02 was 57 mm Hg on room air. Chest X-ray revealed elevation of the right hemidiaphragm, bilateral pleural effusions, greater on the left, an enlarged cardiac shadow (as on previous pictures), and the mediastinum widened to the right. 10 min later she was acutely shocked and had bradycardia. The neck veins were distended. A massive pulmonary embolism was suspected. External cardiac massage and ventilation with 100% oxygen were started and an emergency median sternotomy was done about 15 min later. The pericardium was opened and there was immediate release of 500 ml clear fluid (glucose content 53 mmol/1) which was under pressure. 1500 ml of fluid with the same appearance and glucose content was drained from the right pleural space and 2 litres straw coloured fluid was withdrawn from the left pleural space, compatible with her pancreatitis. No signs of pulmonary embolism were found. Immediately after pericardial drainage the heart resumed spontaneous sinus rhythm. Methylene-blue injected into the subclavian catheter appeared in the superior mediastinal tissues. It was not considered appropriate to search for the perforation because there were no signs of bleeding, and the catheter. was removed. The pericardium and both pleural cavities were drained and the sternum closed. The patient never regained consciousness. An electroencephalogram confirmed brain death, presumably due to anoxia, and the patient died 24 h later. SVC perforation is a life-threatening complication, particularly when large pleural effusions or pericardial tamponade result. It tends to occur hours to days after insertion of the catheter and, clinically, is rarely suspected. The type of catheter used seems unrelated to vessel perforation when catheters with blunt tips are used. Insertion from the left side has a higher morbidity. As Russell and colleagues state, perforation can lead to large pleural effusions but erosion of the mediastinal pleura can cause an isolated right haemothorax or hydrothorax. Fatal cardiac tamponade due to SVC perforation below the pericardial reflection has been described. In our case the catheter perforated a central vein above the pericardial reflection, which resulted in a hydromediastinum and hydrothorax on the right side. The effusate had a much lower glucose content than the TPN solution and we believe that, because of the high osmolarity of the TPN solution, water was attracted into the pericardial cavity, resulting in cardiac tamponade. This occurred in a short time. In suspected TPN fluid-leakage, the infusion should be stopped immediately and pleural and/or pericardial drainage should be instituted as appropriate to avoid osmotic attraction into the pericardial cavity.
(CMV) infection. HLH
was
Department of Paediatrics, St Goran’s Children’s Hospital and Department of Pathology, Karolinska Hospital, Karolinska Institute, S-112 81 Stockholm, Sweden
JAN-INGE HENTER GÖRAN ELINDER OLLE SÖDER
ÅKE ÖST
1. Risdall
RJ, McKenna RW, Nesbit ME, et al. Virus-associated hemophagocytic syndrome: A benign histiocytic proliferation distinct from malignant histiocytosis. Cancer 1979; 44: 993-1002. 2. Ambruso DR, Hays T, Zwartjes WJ, Tubergen DG, Favara BE. Successful treatment of lymphohistiocytic reticulosis with phagocytosis with epipodophyllotoxin VP 16-213. Cancer 1980; 45: 2516-20. 3. Fischer A, Virelizier JL, Arenzana-Seisdedos F, Perez N, Nezelof C, Griscelli C. Treatment of four patients with erythrophagocytic lymphohistiocytosis by a combination of epipodophyllotoxin, steroids, intrathecal methotrexate, and cranial irradiation. Pediatrics 1985; 76: 263-68. 4. Henter J-I, Elinder G, Finkel Y, Soder O. Successful induction with chemotherapy including teniposide in familial erythrophagocytic lymphohistiocytosis. Lancet 1986; ii: 1402. 5. Janka GE. Familial hemophagocytic lymphohistiocytosis. Eur J Pediatr 1983; 140: 221-30.
5623
COMPLICATION OF CENTRAL VENOUS CATHETERISATION
568) report three cases of catheter perforation of the superior vena cava (SVC), two of which were associated with thrombosis. Many complications of SIR,-Dr Russell and colleagues (March 7,
central
venous
p
catheterisation have been described. The
patients).1 Tocino reported nine
cases
EJ Eindhoven, Netherlands
JEANNE BAX CEES JANSVELD JACEK JAKIMOWICZ P. N. HENDEL
1. Eerola R, Kaukinen L,- Kaukinen S. Analysis of 13800 subclavian catheterizations. Acta Anaesthesiol Scand 1985; 29: 193-97. 2. Tocino IM, Watanabe A. Impending catheter perforation of superior vena cava.
vein
AJR
1986; 146: 487-90.
most
and most dangerous complications are pneumothorax, air embolism, thrombosis, and sepsis (overall incidence of 5 % in a common
survey of 13 800
Departments of Pulmonary Medicine, Surgery, and Thoracic and Cardiac Surgery, Catharina Hospital,
of SVC
perforation by central venous catheters.2 She observed, radiographically, mediastinal widening and pleural effusions in all patients, and pericardial effusion in one. Seven effusates had a glucose content greater than 22 mmol/1. We report a fatal case of innominate vein or SVC perforation followed by hydrothorax, hydromediastinum, and pericardial effusion, associated with leakage of total parenteral nutrition (TPN). A 28-year-old woman with acute pancreatitis underwent a cholecystectomy and common bileduct exploration for biliary lithiasis. Therefore TPN was necessary postoperatively. A Viggo ’Secalon-T’ catheter was inserted percutaneously via the right
AIDS AND HUMAN MILK BANK CLOSURES
SiR,—There is debate on whether or not to close human milk banks, on the grounds that preterm infants might contract AIDS from infected donors. The subject has received media coverage; occasionally parents refuse to allow their preterm baby to receive donor milk; and some milk banks have already been shut. No formal Government advice has emerged. The current climate is conducive to hasty decisions, and I wish to draw attention to data from our large multicentre feeding trials,l based at the MRC Dunn Nutrition Unit, which bear on this issue. On average, one-third of the milk volume used by neonatal units is maternal "preterm" milk ;2 the remainder must be supplied as a "back-up diet" (donor breast milk, standard formula, or fortified preterm formula). Donor breast-milk does not meet theoretical
-
She also had a cytomegalothen considered and she was given oral steroids, intravenous teniposide, and intrathecal methotrexate.4 Within a week there was a considerable clinical and laboratory improvement. Foscarnet infusions were given during the second and third week of chemotherapy as a protection against generalised CMV infection. The antiviral therapy did not seem to contribute to the continuous recovery already seen in the first week of chemotherapy. If the girl had instead been classified as VAHS, cytotoxic therapy, which we think was life-saving, would not have been considered. Some of the patients classified as VAHS by Risdall et al,l especially those lacking apparent underlying disease, may have had HLH, although it is difficult to judge because, for example, analyses of lipids and CSF were not presented. Some of the patients receiving azathioprine and prednisone, mainly the renal transplant recipients who had undergone splenectomy, may have had a benign reactive state of histiocytic proliferation with some erythrophagocytosis. This is underlined by the fact that in the latter group only 5 out of 14 patients had hepatomegaly, whereas Janka found hepatomegaly in 94% of the patients with HLH.5 The immunocompromised condition of these patients might have contributed to the aggressive picture in this otherwise harmless reaction. Thus we hesitate to use the diagnosis VAHS, although we admit that the massive histiocytic proliferation in immunocompromised patients is interesting and needs further evaluation. We suggest that the proposed classification of histiocytosis syndromes in children be changed so that HLH and VAHS are considered as the same disease and classified as HLH. The commonly used term "familial", in familial erythrophagocytic lymphohistiocytosis, may be misleading, and we think that haemophagocytic lymphohistiocytosis is a better name for this disease.
hyperplasia with erythrophagocytosis.
subclavian vein, and the catheter tip lay parallel to the walls of the
virus
SVC on the control chest X-ray. Two days later she was dyspnoeic. On the third day she suddenly became- hypotensive and acutely dyspnoeic. She was transferred to an intensive care unit: she was pale and cyanotic, systolic blood pressure was 60-80 mm Hg and .pa02 was 57 mm Hg on room air. Chest X-ray revealed elevation of the right hemidiaphragm, bilateral pleural effusions, greater on the left, an enlarged cardiac shadow (as on previous pictures), and the mediastinum widened to the right. 10 min later she was acutely shocked and had bradycardia. The neck veins were distended. A massive pulmonary embolism was suspected. External cardiac massage and ventilation with 100% oxygen were started and an emergency median sternotomy was done about 15 min later. The pericardium was opened and there was immediate release of 500 ml clear fluid (glucose content 53 mmol/1) which was under pressure. 1500 ml of fluid with the same appearance and glucose content was drained from the right pleural space and 2 litres straw coloured fluid was withdrawn from the left pleural space, compatible with her pancreatitis. No signs of pulmonary embolism were found. Immediately after pericardial drainage the heart resumed spontaneous sinus rhythm. Methylene-blue injected into the subclavian catheter appeared in the superior mediastinal tissues. It was not considered appropriate to search for the perforation because there were no signs of bleeding, and the catheter. was removed. The pericardium and both pleural cavities were drained and the sternum closed. The patient never regained consciousness. An electroencephalogram confirmed brain death, presumably due to anoxia, and the patient died 24 h later. SVC perforation is a life-threatening complication, particularly when large pleural effusions or pericardial tamponade result. It tends to occur hours to days after insertion of the catheter and, clinically, is rarely suspected. The type of catheter used seems unrelated to vessel perforation when catheters with blunt tips are used. Insertion from the left side has a higher morbidity. As Russell and colleagues state, perforation can lead to large pleural effusions but erosion of the mediastinal pleura can cause an isolated right haemothorax or hydrothorax. Fatal cardiac tamponade due to SVC perforation below the pericardial reflection has been described. In our case the catheter perforated a central vein above the pericardial reflection, which resulted in a hydromediastinum and hydrothorax on the right side. The effusate had a much lower glucose content than the TPN solution and we believe that, because of the high osmolarity of the TPN solution, water was attracted into the pericardial cavity, resulting in cardiac tamponade. This occurred in a short time. In suspected TPN fluid-leakage, the infusion should be stopped immediately and pleural and/or pericardial drainage should be instituted as appropriate to avoid osmotic attraction into the pericardial cavity.
(CMV) infection. HLH
was
Department of Paediatrics, St Goran’s Children’s Hospital and Department of Pathology, Karolinska Hospital, Karolinska Institute, S-112 81 Stockholm, Sweden
JAN-INGE HENTER GÖRAN ELINDER OLLE SÖDER
ÅKE ÖST
1. Risdall
RJ, McKenna RW, Nesbit ME, et al. Virus-associated hemophagocytic syndrome: A benign histiocytic proliferation distinct from malignant histiocytosis. Cancer 1979; 44: 993-1002. 2. Ambruso DR, Hays T, Zwartjes WJ, Tubergen DG, Favara BE. Successful treatment of lymphohistiocytic reticulosis with phagocytosis with epipodophyllotoxin VP 16-213. Cancer 1980; 45: 2516-20. 3. Fischer A, Virelizier JL, Arenzana-Seisdedos F, Perez N, Nezelof C, Griscelli C. Treatment of four patients with erythrophagocytic lymphohistiocytosis by a combination of epipodophyllotoxin, steroids, intrathecal methotrexate, and cranial irradiation. Pediatrics 1985; 76: 263-68. 4. Henter J-I, Elinder G, Finkel Y, Soder O. Successful induction with chemotherapy including teniposide in familial erythrophagocytic lymphohistiocytosis. Lancet 1986; ii: 1402. 5. Janka GE. Familial hemophagocytic lymphohistiocytosis. Eur J Pediatr 1983; 140: 221-30.
5623
COMPLICATION OF CENTRAL VENOUS CATHETERISATION
568) report three cases of catheter perforation of the superior vena cava (SVC), two of which were associated with thrombosis. Many complications of SIR,-Dr Russell and colleagues (March 7,
central
venous
p
catheterisation have been described. The
patients).1 Tocino reported nine
cases
EJ Eindhoven, Netherlands
JEANNE BAX CEES JANSVELD JACEK JAKIMOWICZ P. N. HENDEL
1. Eerola R, Kaukinen L,- Kaukinen S. Analysis of 13800 subclavian catheterizations. Acta Anaesthesiol Scand 1985; 29: 193-97. 2. Tocino IM, Watanabe A. Impending catheter perforation of superior vena cava.
vein
AJR
1986; 146: 487-90.
most
and most dangerous complications are pneumothorax, air embolism, thrombosis, and sepsis (overall incidence of 5 % in a common
survey of 13 800
Departments of Pulmonary Medicine, Surgery, and Thoracic and Cardiac Surgery, Catharina Hospital,
of SVC
perforation by central venous catheters.2 She observed, radiographically, mediastinal widening and pleural effusions in all patients, and pericardial effusion in one. Seven effusates had a glucose content greater than 22 mmol/1. We report a fatal case of innominate vein or SVC perforation followed by hydrothorax, hydromediastinum, and pericardial effusion, associated with leakage of total parenteral nutrition (TPN). A 28-year-old woman with acute pancreatitis underwent a cholecystectomy and common bileduct exploration for biliary lithiasis. Therefore TPN was necessary postoperatively. A Viggo ’Secalon-T’ catheter was inserted percutaneously via the right
AIDS AND HUMAN MILK BANK CLOSURES
SiR,—There is debate on whether or not to close human milk banks, on the grounds that preterm infants might contract AIDS from infected donors. The subject has received media coverage; occasionally parents refuse to allow their preterm baby to receive donor milk; and some milk banks have already been shut. No formal Government advice has emerged. The current climate is conducive to hasty decisions, and I wish to draw attention to data from our large multicentre feeding trials,l based at the MRC Dunn Nutrition Unit, which bear on this issue. On average, one-third of the milk volume used by neonatal units is maternal "preterm" milk ;2 the remainder must be supplied as a "back-up diet" (donor breast milk, standard formula, or fortified preterm formula). Donor breast-milk does not meet theoretical