Title
Search
All Issues
9
Year: 2005  Vol. 9   Num. 3  - July/Sept Print:
Case Report
Versão em PDF PDF in Portuguese Texto Text in Portuguese
Severe Epistaxis and Thrombocytopathy in Oncology Patient
Epistaxe Grave e Plaquetopatia em Paciente com Câncer
Author(s):
Lucas Gomes Patrocínio*, Gustavo Brazuna Moura**, Jefferson Batista de Paula Silva**,
José Rodrigues Santos Júnior**, Kalysta de Oliveira Resende***, José Antônio Patrocínio****.
Key words:
epistaxis, thrombocytopathy, surgery, hemostasis.
Abstract:

Introduction: Epistaxis has several causes that can be divided into local and systemic. Among them, hematological diseases present an important role. Objective: We describe a case of severe epistaxis in a patient with cancer associated to thrombocytopathy. We discuss the physiopathology of thrombocytopathy in epistaxis and the treatment performed. Case Report: A 76 year-old male patient presented severe epistaxis due to a thrombocytopathy (functional disturb associated to a quantitative reduction of platelets count), with no laboratorial coagulation alteration. Due to various factors as prostate adenocarcinoma, osseous metastasis, age and chemotherapy, he progressively developed pancytopenia. No success was reached with clinical treatment, so we opted to perform surgical treatment (sphenopalatine, ethmoidal, and internal maxillary arteries). However, due to clinical conditions, the patient died in post anesthesia period. Conclusions: In the present case, it is clear that the complexity to deal with severe epistaxis of systemic causes demands a multidisciplinary approach, including hematologists, otolaryngologists and oncologists to reach therapeutic success, always discussing the risk-benefit of surgical treatment.

INTRODUCTION

Nasal hemorrhage or epistaxis is one of the most frequent of the hemorrhages. Intense vascularization, fragility of nasal mucosa and exposure to trauma area and irritant agents justify that incidence (1). 60% of adult population is estimated to have presented at least one case of epistaxis. Most of epistaxis (90%) occur in the posterior nasal cavity and are easily controlled. Posterior nasal cavity bleeding is a bigger problem, as large bleeding increases the risk of patients (2, 3).

The main epistaxis causes are: traumatisms, upper airway infections, dry and cold air inhalation, nasal allergy, foreign bodies in nasal cavity, tumors, atherosclerosis of the blood vessels, arterial hypertension, coagulopathy and anticoagulant medicine and platelet antiaggregating medicine.

The indicated treatment methods are chemical or electrical cauterization, anterior and posterior packing. Failures on controlling intense and persistent nose bleeding can occur in 10% to 20% of the cases. In those cases, electrical cauterization, embolization or sphenopalatine artery ligation is recommended (3, 4). Ethmoidal arteries ligation, internal maxilla arteries or branches of carotid can also be recommended, but more rarely.

The target of this study is to report a severe case of epistaxis in an oncology patient with associated thrombocytopathy, who died during treatment, calling the attention to systemic factors.

CASE REPORT

R.R.M., 76ys, male, melanoderma, with adenocarcinoma history of non-surgical prostate, was diagnosed about three years ago. He went to hospital with light epistaxis and hemoptoic expectoration, without cough, fever or lung pain. He had osseous metastasis, so radiotherapy on posterior left side of pelvis and chemotherapy with docetaxel and mitoxantrone had been done for three months.

Telangiectasias and diffuse hyperemia of septum of the nose were diagnosed as anterior epistaxis at rhinoscopy. The complete blood count pointed out 8.8g/dl haemoglobin, 123,000 platelets/mm3 and 4,800 leukocytes/mm3. The coagulogram (TAP/INR; TTPA) was normal. It was done anterior nose packing, and then he was allowed to leave the first aid clinic.

He returned after one day, showing severe and continuous epistaxis. A new comprehensive blood count was done and resulted 7.3g/dl haemoglobin, 118.000-platelets/ mm3 and 3,400 leukocytes/mm3. Kidney function was normal. It was also done a new anterior nose packing with gauze, and as bleeding was not interrupted, it was done a posterior nose packing using Foley probe (no.10). And it was transfused 2 IU of concentration of red blood cells, 600 ml of fresh plasma and 7IU of platelets.

On the following day, there was a bleeding maintenance. A surgical treatment was recommended but refused by the patient and his family. It was transfused 3 IU of concentration of red blood cells, 600 ml of fresh plasma and 7 IU of platelets. After signing an approval term, the patient left hospital, returning three days later with moderate epistaxis and in worse general physical condition. He presented 7.4g/dl hemoglobin, 73,000 platelets/mm3 and 5,400 leukocytes/mm3, and was making use of Kanakion® and Transamin®. Then endoscopic cauterization of bilateral sphenopalatine artery was done. After two days, the patient had severe epistaxis again at right, what led to an internal maxillary and anterior and posterior ethmoidal arteries ligation, under general anesthesia, with interruption of bleeding. However, during post-anesthesia recovery period, the patient had cardiorespiratory failure and died afterwards.

DISCUSSION

The multiple causes of epistaxis can be divided into two broad categories - local and systemic. Local causes can be traumatic or mechanical, inflammatory by nasal structural/anatomic diseases, foreign bodies, iatrogenic, surgeries and tumors. Among systemic causes we can find cardiovascular causes (hypertension and atherosclerosis), hematological causes (coagulopathy, platelet disease, leukosis, myeloproliferative diseases), congenital (Osler-Weber-Rendu), hepatic, kidney diseases, and so forth (5).

In this current case, patient presented an oncology disease, as etiology of epistaxis, probably assign to thrombocytopathy (functional disturb associated to a quantitative reduction of platelets count), without laboratory diseases in Coagulation cascade. Patients with these imperfections can present bruises and spontaneous bleeding or even small traumas.

Platelets functional disease can be congenital, caused either by specific gene mutations or they can be acquired because of drug actions, or pathological state, which causes platelet active (6). Qualitative disease acquired from platelets occurs in large numbers, and the ones caused by medication, especially acetylsalicylic acid (aspirin), are more frequent. Some systemic diseases cause platelet functional disease as disseminated vascular coagulation, cardiopulmonary bypass, hepatopathy, atherosclerotic disease, falciform anemia, hemangioma, chronic myeloproliferative disorders, paraproteinemias, aortic aneurysm and uraemia.

90% of oncology patients can show coagulation changes. Among them is platelets aggregation increase, which is the largest activity of procoagulant factors as thrombinase, and X factor, which is, on the other hand, smaller activity of anticoagulant factors.

In the case development, the patient had pancytopenia and coagulation cascade alteration, worsening epistaxis. Probably, chemotherapy associated to medullar invasion counted for that. Chemotherapy, in the past, was much doubted for prostate cancer treatment, because of its toxicity use and difficulty response measure to medication. Thus, it is important to consider the objective response rate, with clinical benefit provided by treatment, remembering its inherent toxicity. There are many different types of chemotherapy side effects (8). Usually, increasing cells are more sensitive. The most important toxic effects are: leukopenia, thrombocytopenia, anemia, alopecia, mucosite, nausea and vomiting (by medication action on specific areas of the nervous system), mucosa thickness reduction (causing inflammation and small ulcerations) (9).

Different types of treatment have been suggested with the purpose of controlling epistaxis, based on its location, etiology and current doctor experience. During initial evaluation, a brief history should be done while first basic support measures and bleeding control are taken. Nasal cavity exam, under anesthesia and topic vasoconstrictor, should be done in detail. This exam is extremely important to find bleeding point and to chose a suitable treatment for each case (3). In the case of previous nosebleed, chemical cauterization, direct electrocoagulation of the bleeding point or even anterior nasal packing is therapeutic alternatives. For posterior, posterior-superior or superior nosebleed, it is necessary posterior nasal packing, what occurs in approximately 48-74% of the cases (10).

In the current case, sphenopalatine artery cauterization via endoscopic endonasal, with which success on bleeding control was not obtained. Some studies show that failure rate can range from 10 to 20% (11). After that, it was made ethmoidal and internal maxillary arteries ligation. Its success rate ranges from 76 to 92%, being the most frequent cause of failure at vase unsuitable identification (12). Apparently, in the exposed case, ligation showed bleeding control, though it was not possible to evaluate it in long term because the patient died by clinical complications. Morbidity rate in this procedure is from 14 to 28% (13, 14).

FINAL COMMENTS

According to the reported case, it is clear that the complexity to deal with epistaxis of systemic causes, which demands multidisciplinary approach, including hematologists, ENT doctors and oncologists to reach therapeutic success, always discussing the risk-benefit of surgical treatment.

BIBLIOGRAPHY

1. Godoy JMP, Batigália F, Paiva JV, Mendes RN, Oliveira JD. Aminaftona no tratamento de epistaxe. Rev Bras Hematol Hemot 2003, 25(1):65-6.

2. Almeida GS, Pinheiro SD, Pinheiro Neto CD. Cauterização endoscópica da artéria esfenopalatina em epistaxe posterior. Arq Otorrinolaringol 2001, 5(2).

3. Balbani APS, Formigoni GGS, Butugan O. Tratamento da epistaxe. Rev Assoc Méd Bras 1999, 45(2):189-93.

4. Stamm AC, Pinto JA, Neto AF, Menon AD. Microsurgery in severe posterior epistaxis. Rhinology 1985, 23:321-5.

5. Patrocínio JA, Castro SC, Freitas RMR, Vital GRF, Sabóia RS. Epistaxe causada por aneurisma intercavernoso traumático. A Folha Médica - Caderno de Otorrinolaringologia 1996, 112(1):107.

6. Nurden AT. Inherited abnormalities of platelets. Thromb Haemost 1999, 82:468-80.

7. Santos AJ, Malheiros SMF, Borges LRR, Dzik C, Nalli DG, Gabbai AA. Acidente vascular cerebral isquêmico após quimioterapia com cisplatina, etoposide e bleomicina. Arq Neuropsiquiatr 2003, 61(1):129-33.

8. Oncotech Oncologia. Disponível em: http://www.oncotech.com.br [acessado em 07/06/2004].

9. Quimioterapia e Cirurgia. [Disponível em: http://www.meaumarci.hpg.ig.com.br/quimioterapia.htm. [acessado em 07/06/2004].

10. Monte ED, Belmont MJ, Wax MK. Management paradigms for posterior epistaxis: a comparison of costs and complications. Otolaryngol Head Neck Surg 1999, 121:103-6.

11. Frikart L, Agrifolio A. Endoscopic treatment of posterior epistaxis. Rhinology 1998, 36:59-61.

12. Patrocínio JA. Ligadura de la artéria maxilar interna utilizando el bisturi pasa-hilo de Patrocínio. A Folha Médica - Caderno de Otorrinolaringologia 1997, 115(92):111-5.

13. Cullen MM, Tami TA. Comparison of internal artery ligation versus embolization for refractory posterior epistaxis. Otolaryngol Head Neck Surg 1998, 118:636-42.

14. Strong EB, Bell DA, Johnson LP, Jacobs JM. Intractable epistaxis. Transnasal ligation vs embolization - efficacy review and cost analysis. Otolaryngol Head Neck Surg 1995, 113:674-8.

  Print:

 

All right reserved. Prohibited the reproduction of papers
without previous authorization of FORL © 1997- 2019