Hemodialysis International 2014; 18:522–561
8 Holubek WJ, Hoffman RS, Goldfarb DS, Nelson LS. Use of hemodialysis and hemoperfusion in poisoned patients. Kidney Int. 2008; 74:1327–1334. 9 Gil HW, Kim SJ, Yang JO, Lee EY, Hong SY. Clinical outcome of hemoperfusion in poisoned patients. Blood Purif. 2010; 30:84–88. 10 Unei H, Ikeda H, Murakami T, Tanigawa K, Kihira K. Detoxication treatment for carbamazepine and lithium overdose. Yakugaku Zasshi. 2008; 128:165–170. 11 Graudins A, Peden G, Dowsett RP. Massive overdose with controlled-release carbamazepine resulting in delayed peak serum concentrations and life-threatening toxicity. Emerg Med. 2002; 14:89–94.
12 Bek K, Koçak S, Ozkaya O, Yilmaz Y, Aydin OF, Tas¸döven CS. Carbamazepine poisoning managed with haemodialysis and haemoperfusion in three adolescents. Nephrology. 2007; 12:33–35. 13 Garlich FM, Goldfarb DS. Have advances in extracorporeal removal techniques changed the indications for their use in poisonings? Adv Chronic Kidney Dis. 2011; 18:172– 179. 14 Churchwell MD, Pasko DA, Smoyer WE, Mueller BA. Enhanced clearance of highly protein-bound drugs by albumin-supplemented dialysate during modeled continuous hemodialysis. Nephrol Dial Transplant. 2009; 24:231–238.
Heparin-induced thrombocytopenia due to heparin lock in a hemodialysis patient: A case report Koon Ming CHAN, Chi Yuen CHEUNG, Ka Foon CHAU Department of Medicine, Queen Elizabeth Hospital, Hong Kong
Abstract Heparin-induced thrombocytopenia (HIT) is a potentially fatal clinical condition which can develop after exposure to unfractionated or low-molecular-weight heparins. Even small doses of heparin such as heparin flushes in hemodialysis catheter can induce the development of HIT. However, the true incidence of heparin lock-related HIT is unknown. We report a 58-year-old woman with acute kidney injury because of obstructive uropathy who developed HIT after heparin-free hemodialysis. She was found to have severe thrombocytopenia with deep vein thrombosis of left lower limb and arterial thrombosis of the right anterior and middle cerebral arteries. The heparin-platelet factor 4 antibody was positive and she was put on plasmapharesis. However, her condition further deteriorated and succumbed shortly. Heparin lock solution in the hemodialysis catheter was believed to be the cause of HIT in our patient. Key words: Hemodialysis, heparin lock, thrombocytopenia
INTRODUCTION Correspondence to: C. Y. Cheung, Department of Medicine, Queen Elizabeth Hospital, 30 Gascoigne Road, Kowloon, Hong Kong. E-mail: [email protected] Conflict of interest: Nil Disclosure of grants or other funding: Nil
Heparin-induced thrombocytopenia (HIT) remains an important diagnosis because of the widespread use of heparin in our daily clinical practice. It is a potentially fatal condition which can develop after exposure to unfractionated or low-molecular-weight heparins
© 2014 International Society for Hemodialysis DOI:10.1111/hdi.12137
555
Case Reports
(LMWH). There are two types of HIT, namely type 1 (HIT 1) and type 2 (HIT 2). HIT 1 is more common and the thrombocytopenia is usually mild and transient. It is a benign condition not associated with risk of thrombosis. On the other hand, HIT 2 is rare but important because of its potential life-threatening thrombotic complications. It is believed to be an immune-mediated disorder, usually occurring more than 5 days of heparin use, and is associated with significant drop in platelet count and new sites of arterial and venous thrombosis. Patients undergoing hemodialysis require heparin during dialysis sessions in order to prevent thrombosis of extracorporeal circuits. Small doses of heparin such as heparin lock solution in the catheter are believed to be sufficient to induce the development of HIT 2. However, the true incidence is unknown because of the limited number of cases in literature.1 Herein, we report a patient suffering from acute kidney injury because of obstructive uropathy who received two sessions of heparin-free hemodialysis via left femoral hemodialysis catheter. She developed deep vein thrombosis of left lower limb 1 week later and was treated with LMWH. However, she was found to have severe thrombocytopenia the next day, which was further complicated with acute fatal ischemic stroke. The cause of HIT in our patient was believed to be related to the heparin lock solution in the hemodialysis catheter.
CASE REPORT A 58-year-old woman with a history of type 2 diabetes mellitus, hypertension and mild renal impairment with baseline serum creatinine 120 μmol/L was admitted to our hospital because of sudden onset of left sided loin pain. Her usual medication included lisinopril, metformin and insulin isophane human. Physical examination was unremarkable except mild left sided loin tenderness. There was no fever. Laboratory data included: hemoglobin 13.7 g/dL, white cell count 18.2 × 109/L, platelet count 285 × 109/L, urea 29.6 mmol/L, creatinine 910 μmol/L, potassium 7.4 mmol/L, sodium 143 mmol/L, bicarbonate 3.9 mmol/L and albumin 44 g/L. Her liver function and coagulation profile was normal. Urgent computed tomography of abdomen showed a 1.1 cm left ureteric stone complicated with hydronephrosis. The diagnosis was acute kidney injury because of obstructive uropathy. Metformin and lisinopril were stopped, and left-sided percutaneous nephrostomy was performed immediately. A hemodialysis catheter was inserted at her left femoral vein and hemodialysis was initiated using heparin-free
556
Figure 1 Cerebral computed tomography showing extensive right fronto-parieto-temporal region infarction.
regimen. After dialysis, 1.2 mL unfractionated heparin (heparin preparation: 1000 units/mL) was loaded at the A-port and 1.3 mL was loaded at the V-port of the hemodialysis catheter. Another session of heparin-free hemodialysis was performed 2 days later. Her renal function gradually improved afterwards. However, she was noted to have sudden onset of left lower limb swelling 1 week after hospitalization. Computed tomography angiogram confirmed acute deep venous thrombosis extending from left popliteal vein to left common iliac vein. Enoxaparin was started and the hemodialysis catheter was removed. She was diagnosed to have thrombocytopenia (platelet count 88 × 109/L) the next day, which became severe (8 × 109/L) when blood test was repeated on the same day. The clinical diagnosis was HIT. Enoxaparin was stopped immediately and an inferior vena cava filter was inserted for the prevention of pulmonary embolism. However, she developed sudden onset of drowsiness with leftsided hemiplegia the next day (power grade 0/5 on left side). Cerebral computed tomography showed extensive right fronto-parieto-temporal region infarction (Figure 1) which was compatible with acute right anterior and middle cerebral artery thrombosis. The heparin-platelet factor 4 (HPF4) antibodies by enzyme-linked immunosorbent assay (ELISA) was positive and she was given a session of plasmapharesis. However, her condition further deteriorated and she succumbed 2 days after stroke.
Hemodialysis International 2014; 18:522–561
Case Reports
DISCUSSION HIT remained a diagnostic challenge because the clinical manifestations can be misleading. In our patient, the deep vein thrombosis was initially thought to be related to the hemodialysis catheter inserted in the left femoral vein. Therefore, the catheter was removed and LMWH was started immediately. However, thrombocytopenia was noted the next day which became more severe when blood test was repeated. Subsequent HPF4 antibody positivity confirmed the presence of HIT 2. As HIT 2 usually occurs between 5 and 14 days after heparin exposure, the temporal relationship suggests that heparin lock solution in the dialysis catheter was the cause of HIT 2 in our patient. Studies have already shown that when dialysis catheters are filled with locking solutions, there is significant risk of overfill with spillage into the systemic circulation which may lead to adverse clinical events.2 Moreover, occurrence of venous thrombosis before the initiation of LMWH also points to the fact that the heparin lock solution alone may already trigger the development of HPF4 antibody and the thrombotic events despite normal platelet count while the subsequent therapeutic doses of LMWH further aggravate the situation, leading to the development of acute massive stroke. The diagnosis of HIT 2 requires combination of clinical assessment and HPF4 immunoassays. The sensitivity of the HPF4 ELISA was 97%, with specificity ranging from 50% to 93%, and a positive correlation was recorded between the level of antibodies to HPF4 and clinical score.3 Absence of HPF4 antibodies can effectively rule out HIT 2. However, its presence has been found in many cases without clinical disease.4 Studies have shown that HPF4 antibodies can be found in patients undergoing hemodialysis with prevalence ranging from 2.8% to 17.9%.5,6 A recent study also showed that 5.6% of Chinese patients on maintenance hemodialysis had positive HPF4 antibodies but none of them developed HIT 2.7 Since the turn-around time of the immunoassays usually take several days, making clinical diagnosis and giving appropriate treatment in a timely fashion even before the availability of HPF4 antibody results is extremely important. If a patient develops deep vein thrombosis and low platelet count with recent heparin exposure, HIT 2 should be the diagnosis unless proven otherwise. However, since thrombocytopenia is common in hospitalized patients receiving heparin, a pretest clinical scoring system, the “4 T’s”, has been developed in order to help to differentiate HIT 2 from other causes for thrombocytopenia in a patient treated with heparin.8 However, it was found that a low pretest score could rule out HIT 2 in most situations but
Hemodialysis International 2014; 18:522–561
the implications of an intermediate or high score varied in different clinical settings.9 Recently, a lateral flow immunoassay (LFIA) for HPF4 complex specific IgG antibodies based on gold nanoparticles was developed. This assay correlates well with ELISA, but false positive results are less frequent. More importantly, LFIA is simple and can exclude HIT within 10 minutes.10 Once the diagnosis of HIT 2 is made, prompt treatment should be given including withdrawal of any form of heparin, including heparin lock in vascular access devices and use of anticoagulation alternatives such as direct thrombin inhibitors, regional citrate dialysis and citrate dialysate. There are only limited case reports concerning the use of plasmapharesis in patients with HIT 2. It is believed that plasmapharesis can remove HPF4 antibodies. However, the limitations of these studies include overdiagnosis of HIT 2 and other potential coexisting causes of thrombocytopenia. However, in situations where anticoagulants are contraindicated, plasmapharesis may be the only salvage procedure in patients with HIT 2. Recently, Tun et al. reported a patient with HIT 2 complicated with intracerebral hemorrhage who was successfully treated with plasmapharesis.11 In conclusion, HIT 2 remains an important diagnosis in patients undergoing hemodialysis and can be caused by small doses of heparin such as heparin lock solution. As the complications can be life threatening, high index of suspicion and early diagnosis of HIT 2 is very important in patients who develop thrombocytopenia after hemodialysis.
Manuscript received November 2013; revised December 2013.
REFERENCES 1 Kadidal VV, Mayo DJ, Horne MK. Heparin-induced thrombocytopenia (HIT) due to heparin flushes: A report of three cases. J Intern Med. 1999; 246:325–329. 2 Agharazii M, Plamondon I, Lebel M, Douville P, Desmeules S. Estimation of heparin leak into the systemic circulation after central venous catheter heparin lock. Nephrol Dial Transplant. 2005; 20:1238–1240. 3 Pouplard C, Amiral J, Borg JY, Laporte-Simitsidis S, Delahousse B, Gruel Y. Decision analysis for use of platelet aggregation test, carbon 14-serotonin release assay, and heparin-platelet factor 4 enzyme-linked immunosorbent assay for diagnosis of heparin-induced thrombocytopenia. Am J Clin Pathol. 1999; 111:700–706. 4 Alberio L. Heparin-induced thrombocytopenia: Some working hypothesis on pathogenesis, diagnostic
557
Hemodialysis International 2014; 18:522–561
5
6
7
8
strategies and treatment. Curr Opin Hematol. 2008; 15:456–464. Sitter T, Spannagl M, Banas B, Schiffl H. Prevalence of heparin- induced PF4-heparin antibodies in hemodialysis patients. Nephron.. 1998; 79:245–246. Palomo I, Pereira J, Alarcon M, et al. Prevalence of heparin-induced antibodies in patients with chronic renal failure undergoing hemodialysis. J Clin Lab Anal. 2005; 19:189–195. Zhao D, Sun X, Yao L, et al. The clinical significance and risk factors of anti-platelet factor 4/heparin antibody on maintenance hemodialysis patients: A two-year prospective follow-up. PLoS ONE. 2013; 8:e62239. Warkentin TE. Heparin-induced thrombocytopenia: Pathogenesis and management. Br J Haematol. 2003; 121:535–555.
9 Lo GK, Juhl D, Warkentin TE, Sigouin CS, Eichler P, Greinacher A. Evaluation of pretest clinical score (4 T’s) for the diagnosis of heparin-induced thrombocytopenia in two clinical settings. J Thromb Haemost. 2006; 4:759– 765. 10 Kolde HJ, Dostatni R, Mauracher S. Rapid and simple IgG specific test for the exclusion of heparin induced thrombocytopenia (HIT). Clin Chem Lab Med. 2011; 49:2065– 2068. 11 Tun NM, Bo ZM, Ahluwalia M, Guevara E, Villani GM. A rare case of intracerebral hemorrhage complicating heparin-induced thrombocytopenia with thrombosis: A clinical dilemma ameliorated by novel use of plasmapheresis. Int J Hematol. 2012; 96:513–515.
A miniseries of spontaneous intramural esophageal hematoma in hemodialysis patients: A rare cause of dysphagia Vinod KUMAR, Mallikarjuna HM, Gokulnath Department of Nephrology, St. John’s Medical College and Hospital, Bangalore, India
Abstract Intramural esophageal hematoma (IEH) is an uncommon clinical condition, with a prognosis that is essentially benign. In most cases, a predisposing factor may be seen, with the most common being the history of esophagic instrumentation, food impactions, and thrombocytopenia. We report a miniseries of 3 patients on hemodialysis, who developed IEH. All 3 of them presented with sudden onset and progressively worsening dysphagia and hematemesis. Diagnosis of IEH was established by upper gastrointestinal endoscopy. All patients were managed conservatively, and symptoms of dysphagia and chest pain improved within 6–8 days. Good resolution of hematoma was noted by repeat endoscopy within 2–3 weeks. The reported case of IEH in hemodialysis patients is rare and needs to be identified early when patients present with dysphagia, as anticoagulation during hemodialysis would possibly worsen the clinical condition, the course of which is otherwise benign. Key words: Hematoma, hemodialysis, endoscopy, dysphagia
Correspondence to: Gokulnath, MD, DM, DNB, FRCP, St. John’s Medical College and Hospital, Bangalore 560034, India. E-mail: [email protected] Conflict of interest: None. Disclosure: None.
INTRODUCTION Intramural esophageal hematoma (IEH) is an uncommon clinical condition, with a prognosis that is essentially benign with very few cases reported in hemodialysis
© 2014 International Society for Hemodialysis DOI:10.1111/hdi.12143
558
8 Holubek WJ, Hoffman RS, Goldfarb DS, Nelson LS. Use of hemodialysis and hemoperfusion in poisoned patients. Kidney Int. 2008; 74:1327–1334. 9 Gil HW, Kim SJ, Yang JO, Lee EY, Hong SY. Clinical outcome of hemoperfusion in poisoned patients. Blood Purif. 2010; 30:84–88. 10 Unei H, Ikeda H, Murakami T, Tanigawa K, Kihira K. Detoxication treatment for carbamazepine and lithium overdose. Yakugaku Zasshi. 2008; 128:165–170. 11 Graudins A, Peden G, Dowsett RP. Massive overdose with controlled-release carbamazepine resulting in delayed peak serum concentrations and life-threatening toxicity. Emerg Med. 2002; 14:89–94.
12 Bek K, Koçak S, Ozkaya O, Yilmaz Y, Aydin OF, Tas¸döven CS. Carbamazepine poisoning managed with haemodialysis and haemoperfusion in three adolescents. Nephrology. 2007; 12:33–35. 13 Garlich FM, Goldfarb DS. Have advances in extracorporeal removal techniques changed the indications for their use in poisonings? Adv Chronic Kidney Dis. 2011; 18:172– 179. 14 Churchwell MD, Pasko DA, Smoyer WE, Mueller BA. Enhanced clearance of highly protein-bound drugs by albumin-supplemented dialysate during modeled continuous hemodialysis. Nephrol Dial Transplant. 2009; 24:231–238.
Heparin-induced thrombocytopenia due to heparin lock in a hemodialysis patient: A case report Koon Ming CHAN, Chi Yuen CHEUNG, Ka Foon CHAU Department of Medicine, Queen Elizabeth Hospital, Hong Kong
Abstract Heparin-induced thrombocytopenia (HIT) is a potentially fatal clinical condition which can develop after exposure to unfractionated or low-molecular-weight heparins. Even small doses of heparin such as heparin flushes in hemodialysis catheter can induce the development of HIT. However, the true incidence of heparin lock-related HIT is unknown. We report a 58-year-old woman with acute kidney injury because of obstructive uropathy who developed HIT after heparin-free hemodialysis. She was found to have severe thrombocytopenia with deep vein thrombosis of left lower limb and arterial thrombosis of the right anterior and middle cerebral arteries. The heparin-platelet factor 4 antibody was positive and she was put on plasmapharesis. However, her condition further deteriorated and succumbed shortly. Heparin lock solution in the hemodialysis catheter was believed to be the cause of HIT in our patient. Key words: Hemodialysis, heparin lock, thrombocytopenia
INTRODUCTION Correspondence to: C. Y. Cheung, Department of Medicine, Queen Elizabeth Hospital, 30 Gascoigne Road, Kowloon, Hong Kong. E-mail: [email protected] Conflict of interest: Nil Disclosure of grants or other funding: Nil
Heparin-induced thrombocytopenia (HIT) remains an important diagnosis because of the widespread use of heparin in our daily clinical practice. It is a potentially fatal condition which can develop after exposure to unfractionated or low-molecular-weight heparins
© 2014 International Society for Hemodialysis DOI:10.1111/hdi.12137
555
Case Reports
(LMWH). There are two types of HIT, namely type 1 (HIT 1) and type 2 (HIT 2). HIT 1 is more common and the thrombocytopenia is usually mild and transient. It is a benign condition not associated with risk of thrombosis. On the other hand, HIT 2 is rare but important because of its potential life-threatening thrombotic complications. It is believed to be an immune-mediated disorder, usually occurring more than 5 days of heparin use, and is associated with significant drop in platelet count and new sites of arterial and venous thrombosis. Patients undergoing hemodialysis require heparin during dialysis sessions in order to prevent thrombosis of extracorporeal circuits. Small doses of heparin such as heparin lock solution in the catheter are believed to be sufficient to induce the development of HIT 2. However, the true incidence is unknown because of the limited number of cases in literature.1 Herein, we report a patient suffering from acute kidney injury because of obstructive uropathy who received two sessions of heparin-free hemodialysis via left femoral hemodialysis catheter. She developed deep vein thrombosis of left lower limb 1 week later and was treated with LMWH. However, she was found to have severe thrombocytopenia the next day, which was further complicated with acute fatal ischemic stroke. The cause of HIT in our patient was believed to be related to the heparin lock solution in the hemodialysis catheter.
CASE REPORT A 58-year-old woman with a history of type 2 diabetes mellitus, hypertension and mild renal impairment with baseline serum creatinine 120 μmol/L was admitted to our hospital because of sudden onset of left sided loin pain. Her usual medication included lisinopril, metformin and insulin isophane human. Physical examination was unremarkable except mild left sided loin tenderness. There was no fever. Laboratory data included: hemoglobin 13.7 g/dL, white cell count 18.2 × 109/L, platelet count 285 × 109/L, urea 29.6 mmol/L, creatinine 910 μmol/L, potassium 7.4 mmol/L, sodium 143 mmol/L, bicarbonate 3.9 mmol/L and albumin 44 g/L. Her liver function and coagulation profile was normal. Urgent computed tomography of abdomen showed a 1.1 cm left ureteric stone complicated with hydronephrosis. The diagnosis was acute kidney injury because of obstructive uropathy. Metformin and lisinopril were stopped, and left-sided percutaneous nephrostomy was performed immediately. A hemodialysis catheter was inserted at her left femoral vein and hemodialysis was initiated using heparin-free
556
Figure 1 Cerebral computed tomography showing extensive right fronto-parieto-temporal region infarction.
regimen. After dialysis, 1.2 mL unfractionated heparin (heparin preparation: 1000 units/mL) was loaded at the A-port and 1.3 mL was loaded at the V-port of the hemodialysis catheter. Another session of heparin-free hemodialysis was performed 2 days later. Her renal function gradually improved afterwards. However, she was noted to have sudden onset of left lower limb swelling 1 week after hospitalization. Computed tomography angiogram confirmed acute deep venous thrombosis extending from left popliteal vein to left common iliac vein. Enoxaparin was started and the hemodialysis catheter was removed. She was diagnosed to have thrombocytopenia (platelet count 88 × 109/L) the next day, which became severe (8 × 109/L) when blood test was repeated on the same day. The clinical diagnosis was HIT. Enoxaparin was stopped immediately and an inferior vena cava filter was inserted for the prevention of pulmonary embolism. However, she developed sudden onset of drowsiness with leftsided hemiplegia the next day (power grade 0/5 on left side). Cerebral computed tomography showed extensive right fronto-parieto-temporal region infarction (Figure 1) which was compatible with acute right anterior and middle cerebral artery thrombosis. The heparin-platelet factor 4 (HPF4) antibodies by enzyme-linked immunosorbent assay (ELISA) was positive and she was given a session of plasmapharesis. However, her condition further deteriorated and she succumbed 2 days after stroke.
Hemodialysis International 2014; 18:522–561
Case Reports
DISCUSSION HIT remained a diagnostic challenge because the clinical manifestations can be misleading. In our patient, the deep vein thrombosis was initially thought to be related to the hemodialysis catheter inserted in the left femoral vein. Therefore, the catheter was removed and LMWH was started immediately. However, thrombocytopenia was noted the next day which became more severe when blood test was repeated. Subsequent HPF4 antibody positivity confirmed the presence of HIT 2. As HIT 2 usually occurs between 5 and 14 days after heparin exposure, the temporal relationship suggests that heparin lock solution in the dialysis catheter was the cause of HIT 2 in our patient. Studies have already shown that when dialysis catheters are filled with locking solutions, there is significant risk of overfill with spillage into the systemic circulation which may lead to adverse clinical events.2 Moreover, occurrence of venous thrombosis before the initiation of LMWH also points to the fact that the heparin lock solution alone may already trigger the development of HPF4 antibody and the thrombotic events despite normal platelet count while the subsequent therapeutic doses of LMWH further aggravate the situation, leading to the development of acute massive stroke. The diagnosis of HIT 2 requires combination of clinical assessment and HPF4 immunoassays. The sensitivity of the HPF4 ELISA was 97%, with specificity ranging from 50% to 93%, and a positive correlation was recorded between the level of antibodies to HPF4 and clinical score.3 Absence of HPF4 antibodies can effectively rule out HIT 2. However, its presence has been found in many cases without clinical disease.4 Studies have shown that HPF4 antibodies can be found in patients undergoing hemodialysis with prevalence ranging from 2.8% to 17.9%.5,6 A recent study also showed that 5.6% of Chinese patients on maintenance hemodialysis had positive HPF4 antibodies but none of them developed HIT 2.7 Since the turn-around time of the immunoassays usually take several days, making clinical diagnosis and giving appropriate treatment in a timely fashion even before the availability of HPF4 antibody results is extremely important. If a patient develops deep vein thrombosis and low platelet count with recent heparin exposure, HIT 2 should be the diagnosis unless proven otherwise. However, since thrombocytopenia is common in hospitalized patients receiving heparin, a pretest clinical scoring system, the “4 T’s”, has been developed in order to help to differentiate HIT 2 from other causes for thrombocytopenia in a patient treated with heparin.8 However, it was found that a low pretest score could rule out HIT 2 in most situations but
Hemodialysis International 2014; 18:522–561
the implications of an intermediate or high score varied in different clinical settings.9 Recently, a lateral flow immunoassay (LFIA) for HPF4 complex specific IgG antibodies based on gold nanoparticles was developed. This assay correlates well with ELISA, but false positive results are less frequent. More importantly, LFIA is simple and can exclude HIT within 10 minutes.10 Once the diagnosis of HIT 2 is made, prompt treatment should be given including withdrawal of any form of heparin, including heparin lock in vascular access devices and use of anticoagulation alternatives such as direct thrombin inhibitors, regional citrate dialysis and citrate dialysate. There are only limited case reports concerning the use of plasmapharesis in patients with HIT 2. It is believed that plasmapharesis can remove HPF4 antibodies. However, the limitations of these studies include overdiagnosis of HIT 2 and other potential coexisting causes of thrombocytopenia. However, in situations where anticoagulants are contraindicated, plasmapharesis may be the only salvage procedure in patients with HIT 2. Recently, Tun et al. reported a patient with HIT 2 complicated with intracerebral hemorrhage who was successfully treated with plasmapharesis.11 In conclusion, HIT 2 remains an important diagnosis in patients undergoing hemodialysis and can be caused by small doses of heparin such as heparin lock solution. As the complications can be life threatening, high index of suspicion and early diagnosis of HIT 2 is very important in patients who develop thrombocytopenia after hemodialysis.
Manuscript received November 2013; revised December 2013.
REFERENCES 1 Kadidal VV, Mayo DJ, Horne MK. Heparin-induced thrombocytopenia (HIT) due to heparin flushes: A report of three cases. J Intern Med. 1999; 246:325–329. 2 Agharazii M, Plamondon I, Lebel M, Douville P, Desmeules S. Estimation of heparin leak into the systemic circulation after central venous catheter heparin lock. Nephrol Dial Transplant. 2005; 20:1238–1240. 3 Pouplard C, Amiral J, Borg JY, Laporte-Simitsidis S, Delahousse B, Gruel Y. Decision analysis for use of platelet aggregation test, carbon 14-serotonin release assay, and heparin-platelet factor 4 enzyme-linked immunosorbent assay for diagnosis of heparin-induced thrombocytopenia. Am J Clin Pathol. 1999; 111:700–706. 4 Alberio L. Heparin-induced thrombocytopenia: Some working hypothesis on pathogenesis, diagnostic
557
Hemodialysis International 2014; 18:522–561
5
6
7
8
strategies and treatment. Curr Opin Hematol. 2008; 15:456–464. Sitter T, Spannagl M, Banas B, Schiffl H. Prevalence of heparin- induced PF4-heparin antibodies in hemodialysis patients. Nephron.. 1998; 79:245–246. Palomo I, Pereira J, Alarcon M, et al. Prevalence of heparin-induced antibodies in patients with chronic renal failure undergoing hemodialysis. J Clin Lab Anal. 2005; 19:189–195. Zhao D, Sun X, Yao L, et al. The clinical significance and risk factors of anti-platelet factor 4/heparin antibody on maintenance hemodialysis patients: A two-year prospective follow-up. PLoS ONE. 2013; 8:e62239. Warkentin TE. Heparin-induced thrombocytopenia: Pathogenesis and management. Br J Haematol. 2003; 121:535–555.
9 Lo GK, Juhl D, Warkentin TE, Sigouin CS, Eichler P, Greinacher A. Evaluation of pretest clinical score (4 T’s) for the diagnosis of heparin-induced thrombocytopenia in two clinical settings. J Thromb Haemost. 2006; 4:759– 765. 10 Kolde HJ, Dostatni R, Mauracher S. Rapid and simple IgG specific test for the exclusion of heparin induced thrombocytopenia (HIT). Clin Chem Lab Med. 2011; 49:2065– 2068. 11 Tun NM, Bo ZM, Ahluwalia M, Guevara E, Villani GM. A rare case of intracerebral hemorrhage complicating heparin-induced thrombocytopenia with thrombosis: A clinical dilemma ameliorated by novel use of plasmapheresis. Int J Hematol. 2012; 96:513–515.
A miniseries of spontaneous intramural esophageal hematoma in hemodialysis patients: A rare cause of dysphagia Vinod KUMAR, Mallikarjuna HM, Gokulnath Department of Nephrology, St. John’s Medical College and Hospital, Bangalore, India
Abstract Intramural esophageal hematoma (IEH) is an uncommon clinical condition, with a prognosis that is essentially benign. In most cases, a predisposing factor may be seen, with the most common being the history of esophagic instrumentation, food impactions, and thrombocytopenia. We report a miniseries of 3 patients on hemodialysis, who developed IEH. All 3 of them presented with sudden onset and progressively worsening dysphagia and hematemesis. Diagnosis of IEH was established by upper gastrointestinal endoscopy. All patients were managed conservatively, and symptoms of dysphagia and chest pain improved within 6–8 days. Good resolution of hematoma was noted by repeat endoscopy within 2–3 weeks. The reported case of IEH in hemodialysis patients is rare and needs to be identified early when patients present with dysphagia, as anticoagulation during hemodialysis would possibly worsen the clinical condition, the course of which is otherwise benign. Key words: Hematoma, hemodialysis, endoscopy, dysphagia
Correspondence to: Gokulnath, MD, DM, DNB, FRCP, St. John’s Medical College and Hospital, Bangalore 560034, India. E-mail: [email protected] Conflict of interest: None. Disclosure: None.
INTRODUCTION Intramural esophageal hematoma (IEH) is an uncommon clinical condition, with a prognosis that is essentially benign with very few cases reported in hemodialysis
© 2014 International Society for Hemodialysis DOI:10.1111/hdi.12143
558
