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Case Report
A. Suppiah E. P. Perry
Department of Surgery, Scarborough General Hospital, Scarborough, YO12 6QL
Correspondence to: A. Suppiah (Mr Perry’s office), Department of Surgery, Scarborough General Hospital, Woodlands Drive, Scarborough, YO12 6QL Email: aravindsuppiah@hotmail.com
A 43-year-old man was admitted with jaundice six days following phenol injection sclerotherapy for haemorrhoids. He was diagnosed with a phenol-induced hepatitis. Although he remained well, liver function tests only returned to normal after six months. Systemic absorption of phenol has been reported with ingestion, upper airway and excessive cutaneous exposure but not as a complication of haemorrhoidal injection sclerotherapy. Hepatic involvement is also rare and usually the result of ongoing sepsis. We report the unique case of a patient presenting with jaundice secondary to chemical hepatitis, following systemic absorption of phenol at injection sclerotherapy. This case highlights the importance of clinical awareness of not only the infective complications of injection sclerotherapy but also the potential for phenol to be absorbed systemically with severe consequences. A brief overview of symptoms of phenol toxicity is included
Keywords: Haemorrhoids, sclerotherapy, phenol, complications, hepatic effects Surgeon, 1 February 2005, 43-44
Haemorrhoids are common problems accounting for up to 50% of attendances in rectal clinics.1 Injection sclerotherapy is regarded as a safe and effective outpatient treatment of first and second degree haemorrhoids. Complications of injection sclerotherapy are rare but may be life-threatening. Most reported complications are due to introduction of infection by this technique. However, there is a lack of awareness of phenol as a potentially lethal toxic agent. We report a case of a patient who presented initially with jaundice due to systemic absorption of phenol as a complication of injection sclerotherapy. A brief overview of symptoms of phenol toxicity is included.
A 43-year-old previously fit male National Park Ranger was seen in the outpatient clinic complaining of a five-year history of intermittent rectal bleeding and pruritus. Proctoscopy showed second-degree haemorrhoids at 3, 7 and 11 o’clock positions. These were treated with good results with 2ml 5% phenol injection at each haemorrhoid. He received regular injections in the subsequent months with no complications. During his last injection, he experienced stabbing pains radiating to his penis, which he did not report at the time. He developed haematuria and backache later that evening. He was reviewed by his general practitioner who prescribed a course of antibiotics (amoxicillin) for presumed urinary tract infection. He was admitted to hospital six days later when his general practitioner found him jaundiced.
On admission, he was apyrexial and jaundiced. There was mild right upper quadrant tenderness and rectal examination was unremarkable. Haematological results showed a haemoglobin of 15.8 g/dL (normal 13-18), a haematocrit of 43%, a mild leukocytosis, WCC 14.4 x 109/L (normal 4-11), and low platelets 63 x 109/L (normal 150-400). Both the serum urea, 25.7 mmol/L (normal 2.8-7.6), and creatinine of 171 umol/L (normal 70-133) were raised. The bilirubin, 110 µmol/l (normal 3-17), alkaline phospatase, 301 IU/L (normal 45-122) and alanine aminotransferase of 64 U/L (normal 10-44), were also raised. His INR was 1.1 but serum albumin was low at 31 g/L (normal 38-47). C-reactive protein was elevated at 264 (normal <6).
Hepatitis serology and autoantibody screening were negative. Ultrasonography showed a normal liver and duct system while Doppler studies showed normal hepatic and portal vein flow. He was diagnosed with phenol-induced hepatotoxicity with associated transient renal failure. He responded to conservative treatment and was discharged after a week in hospital. Liver function tests on discharge were improving but still abnormal. He remained well during subsequent reviews in the outpatient clinic. However, liver function tests only returned to normal after six months.
Haemorrhoids account for a significant number of consultations in gastrointestinal clinics and up to 50% of consultations in rectal clinics.1 The incidence of haemorrhoids in the United States general population is 4.4%. Furthermore, up to 88% in people undergoing endoscopic examination of the rectum have haemorrhoids.2,3 Various treatments are used to deal with haemorrhoids including injection sclerotherapy, cryotherapy, infrared coagulation, rubber band ligation, stapling and haemorrhoidectomy.4 Injection sclerotherapy is a well established treatment for primary and secondary haemorrhoids, documented as far back as 1903.5 It involves the submucosal injection of an oily phenol solution causing painless mucosal fixation to the underlying muscle by fibrosis. The correct placement of the injection is characterised by a ‘striation sign’ as described by Goligher (1984).6
Complications of injection sclerotherapy are rare but may be life-threatening. They are caused by introduction of infection into local and retroperitoneal structures. The incidence of bacteraemia post-injection sclerotherapy was 8% in one series although no adverse symptoms were reported.7 Previous documented complications include urological sepsis (prostatism, prostatic abscess, epididymitis, urinary-perineal fistula), skin necrosis, necrotising fasciitis, retroperitoneal sepsis and one case of hepatic abscesses.8-11 Although infective complications are increasingly recognised, there is lack of recognition of the symptoms of phenol toxicity and its consequences.
Phenol is a colourless or faintly pink crystal with a characteristic odour. Its metabolites are excreted in the urine occasionally causing a green colour. Phenol used in injection sclerotherapy is a 5% solution in arachis oil. Two to five millilitres of this solution is injected submucosally to each haemorrhoid.12 Early toxicity causes depressed consciousness, cardiac arrhythmias, acidosis, methaemoglobinaemia, epiglottitis and laryngoedema. Later complications include pulmonary oedema, hepatic failure and renal failure. Previously reported cases of toxicity were due to ingestion or cutaneous absorption.12 Only one case of phenol toxicity from injection sclerotherapy, causing urinary symptoms and impotence lasting for one year, has been reported.13
Hepatic involvement is especially rare in injection sclerotherapy. Documented complications have been the result of ongoing sepsis, not phenol hepatitis. A single case of a hepatic abscesses, as a result of injection sclerotherapy, has been documented. However, the patient presented with a febrile illness rather than jaundice (Bilirubin was 21 µmol/l).11
This case introduces two new clinical aspects. Firstly, jaundice as a complication of injection sclerotherapy. Secondly, this is the first case of systemic absorption of phenol during injection sclerotherapy leading to hepatic toxicity. In conclusion, it is vitally important for every clinician to be aware of not only the infective complications of injection sclerotherapy, but also the symptoms of phenol toxicity and its recognition as a toxic chemical agent.
Copyright 3 December 2004
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