A case report of morbidly obese patient who presented with respiratory failure

Dr Sangram Patil, Specialist Registrar in ITU,

Morriston Hospital, Swansea, SA6 6PU.

Case summary:

A 55-year gentleman with weight 220Kg presented to hospital with increasing shortness of breath for few weeks. His background medical history was type 2 diabetes mellitus, right-sided heart failure, chronic type 2 respiratory failure, sleep apnoea, recent increase in lower limb swelling, orthopnea and paroxysmal nocturnal dyspnoea. His regular medications were furosemide, simvastatin, metformin and co-codamol.

The reason for his presentation to hospital was probably non-infective exacerbation of type 2 respiratory failure. His blood gas in casualty department showed hypoxia with respiratory acidosis (pH7.30, pO2 7.6 kPa, pCO2 10.8 kPa). His bicarbonate level was 12.7mmol/L. Soon he deteriorated on respiration and blood gases deteriorated to pH 7.1, pO2 7.82 and pCO2 14.5 kPa. This patient was referred to ITU team for consideration for non-invasive ventilation.

On admission to ITU the patient was supported with non-invasive ventilation BiPAP- PEEP of 10 mbar and pressure support of 22 mbar on 70% inspired oxygen concentration. He had very poor air entry in chest bilaterally. In spite of high non-invasive support he continued to deteriorate. His pCO2 reached to 15.6 mbar. His airway assessment showed almost no neck, Mallampatti class 4 view of pharynx, very little neck extension, inability to identify cricoid and thyroid cartilages.

Decision was taken to invasively ventilate this patient. Awake fiberoptic ventilation was planned. After local anaesthesia to airway with lignocaine spray and jelly, fiberoptic scope was passed down the nose. The patient started bleeding in his nose and became uncooperative. It became difficult to suck out the throat and visualize larynx. So, the decision was taken to transfer him to theatre and perform fiberoptic intubation under inhalational induction.

Meanwhile, patient received two boluses of furosemide 80mg to offload his right heart. He was transferred to theatre with full monitoring. Inhalational induction with sevofluorane and 100% oxygen was done. Direct laryngoscopy performed when patient was sufficiently under anaesthesia showed grade 2 view of larynx. He was intubated with size 7 ETT due to difficulty in getting a bigger size tube into his trachea. The patient was transferred back to ITU and ventilated with BiPAP mode.

This gentleman posed very difficult technical problems on ITU. It was almost impossible to move him for any procedures on ITU for example for chest X-ray. Transthoracic echocardiography did not show any sensible view at all. He needed high level of ventilatory support with 100% oxygen and PEEP of 18 mbar to keep his oxygen saturations at around 90%. Due to his agitation he was started on remifentanyl and propofol sedation. He developed hypotension from sedation. So, we switched him to midazolam sedation.

After multiple failed attempts at confirming right placement of nasogastric tube, pH method of NG aspirate was used to confirm the placement, as it was impossible to X-ray his chest due to massive size of his chest.

This patient subsequently developed chest infection and deteriorated chest wise. It was decided after a week of intensive therapy that, due to irreversible nature of his cardio respiratory condition, it was not appropriate to resuscitate this patient in case of cardiac arrest. We put limits to his treatment and decided not to escalate his management any further. The plans to perform trans-oesophageal echo were cancelled due to eminent technical problems with it.

This patient continued deteriorating and did not respond to intensive interventions at any point during his ITU stay. The decision was made to withdraw life supports. The patient died immediately after withdrawal of intensive therapy.

Discussion:

Clinical investigations addressing the care of the critically ill, morbidly obese patient are scarce.

Extreme obesity is frequently associated with life-threatening cardiopulmonary disease and presents substantial obstacles to the delivery of routine care.

Morbidly obese patients dedicate a disproportionately high percentage of total O₂ to conduct respiratory work, even during quiet breathing. This relative inefficiency suggests a decreased ventilatory reserve and a predisposition to respiratory failure in the setting of even mild pulmonary or systemic insults.¹

Duarte, Alexander G et al in their study on outcome in morbidly obese ventilated patients have shown increased mortality if the patients did not respond well to NIV and needed invasive ventilation.²A total of 33 patients were treated with non-invasive ventilation (NIV), of which 21 avoided intubation (NIV success) and 12 required intubation (NIV failure). Mean body mass index for the NIV success group was significantly less than for the NIV failure group. Significant improvements in pH and Paco2 were noted for the invasive mechanical ventilation and NIV success groups. No improvements in gas exchange were noted in the NIV failure group. Of patients treated with NIV, 36% required intubation.

In a case report by Masashi Nishikawa et al concluded that basic problem leading to respiratory failure in their patient was morbid obesity, body weight reduction was considered to be mandatory. The caloric intake of a morbidly obese patient was limited to 1000 kcal·day⁻¹, resulting in body weight reduction by 50kg during the patient's stay on the intensive care unit. The patient was successfully extubated on ICU day 35. ³

Philippe Juvin et al have reported a difficult intubation rate of 15.5% in obese patients and 2.2% in lean patients.⁴ Llimited neck mobility and mouth opening accounted for most cases of difficult intubation in obese subjects.⁵ Short sternomental distance, receding mandible, and prominent teeth have been advanced as potential causes for difficult intubation.

The potential problems with critical care of morbidly obese patients are ⁶-

Difficult airway management

Difficult ventilation

Difficult IV access

Pharmacological considerations especially for sedation

Radiological procedures and transfer difficulties

Nutritional requirements

Nursing care

Conclusion:

From our case report we conclude that morbidly obese critically ill patients present with many technical and management issues. They are difficult to handle physically due to their size and it may be very difficult to transfer, investigate and nurse these patients. They might present with medical problems associated with morbid obesity which puts them at high risk of adverse outcome. Management of this group of patients needs a careful team approach and additional technical support.

References:

1. John P Kress et al, The impact of morbid obesity on oxygen cost of breathing at rest. Am. J. Respir. Crit. Care Med., Volume 160, Number 3, September 1999, 883-886

2. Duarte, Alexander G et al, Outcomes of morbidly obese patients requiring mechanical ventilation for acute respiratory failure. Critical Care Medicine. 35(3):732-737, March 2007.

3. Masashi Nishikawa et al- Respiratory failure due to morbid obesity in a patient with Prader-Willi syndrome: an experience of long-term mechanical ventilation, Volume 20, Number 4 / November, 2006, 300-303.

4. Philippe Juvin et al, difficult tracheal intubation is more common in obese than in Lean Patients, Anesth Analg 2003;97:595-600.

5. Williamson JA, Webb RK, Szekely S, Gillies ER, Dreosti AV. The Australian Incident Monitoring Study. Difficult intubation: an analysis of 2,000 incident reports. Anaesth Intensive Care 1993;21:602-607.

6. Clinical Approach to the Critically III, Morbidly Obese Patient American

Journal of Respiratory and Critical Care Medicine, Mar 1, 2004 by El-

Solh, Ali A.

Intensive care management of a patient who had cardiac arrest intra-operatively

Case summary:

A 68 years old gentleman was admitted on intensive care unit following cardiac arrest immediately on induction of anaesthesia. His background medical problems were hypertension and hypothyroidism treated well. He had undergone total laryngectomy for carcinoma of larynx two years prior. He had a permanent tracheostomy with provox valve in place. He was due to have Dupuytren's fasciotomy.

The anaesthetist in theatre put an axillary block using 20 ml of 1% lignocaine and 0.25% bupivacaine each. The patient received fentanyl 100 microgram and midazolam 2 mg to facilitate the block. The tracheostomy tube was replaced with size 7 laryngeal tube while patient was awake using 1% lignocaine spray. After confirming the stable haemodynamic status, general anaesthesia was induced with propofol 120 mg and atracurium 40 mg. Immediately on induction (within few seconds) patient desaturated to SpO2 of 50% on 100 oxygen, the chest became very wheezy and patient had a cardiac arrest. The laryngeal tube became blocked with yellow coloured sputum, so tube was changed to size 5 microlaryngeal tube.

Initially it was PEA arrest. Immediate CPR with adrenaline was administered, after which the rhythm changed to bradycardia and asystole. After third cycle of adrenaline and CPR the rhythm changed to VF. He was shocked with 150J which converted him to sinus tachycardia and the cardiac output was back. He needed metaraminol boluses and adrenaline infusion to maintain the good blood pressure. In theatre 50 ml of intralipid 20% was administered intravenously in an attempt to treat possible local anaesthetic toxicity. He also received doses of hydrocortisone and chlorphenyramine maleate.

Later the patient was transferred to intensive care for further management. After multidisciplinary discussion the probable causes for the cardiac arrest were thought to be-

1. Local anaesthetic toxicity- was unlikely due to the lower than maximum doses used for axillary block.

2. Troponin T of 1.1 microgram/l- might have been due to cardiac arrest or CPR, unlikely due to MI

3. Anaphylaxis to induction agents was questioned due to time of occurrence of arrest (within seconds of induction)

4. Probably airway obstruction from thick airway secretions was a possibility

The patient developed high white cell count of 30,000/cc and became dependent on high doses of ionotropes the next day.

Blood samples were sent to lab to measure local anaesthetic levels. Serum samples for tryptase levels were sent at 1, 6, 24 and 72 hours.

This patient remained on intensive care support for long period of time, remained very slow to wake up. He gradually improved consciousness wise and was transferred to rehabilitation unit for further care.

The drug levels came back as within therapeutic range, whereas serum tryptase levels were raised. As this patient had received propofol in the past and also on ITU this time for sedation without any problems, it was assumed that the anaphylaxis was due to atracurium. As his clinical condition was not good enough it was decided not to refer him to allergy clinic at that point. It was mentioned in his clinical notes not to administer any muscle relaxants in future without prior full assessment.

Discussion:

Many improvements have been seen in monitoring techniques, the widespread adoption of medical practice guidelines and patient care over the last two decades. So, many authors believe that the frequency of anaesthesia-related cardiac arrest and its mortality have declined over recent decades (1). Perioperative cardiac arrests were relatively higher in neonates, infants, elderly and in males with severe underlying disease and under emergency surgery. All anaesthesia-related cardiac arrests were related to airway management and medication administration which is important for prevention strategies (2).

Positive mast cell tryptase = lgE mediated reaction (i.e., anaphylaxis). Negative mast cell tryptase tests are only rarely associated with positive skin tests and antibody tests. While, if taken at the correct time, they usually mean anaphylaxis has not occurred. If tryptase is positive, the patient needs skin testing to identify the agent responsible. This needs to be done 4-6 weeks after the reaction (3).

Intravenous administration of adrenaline is hazardous and should be given in a dilution of at least 1:10 000 (never 1:1000). Intravenous injection of adrenaline must be reserved for patients with profound shock that is immediately life-threatening and for special indications, e.g. during anaesthesia. The injection should be given as slowly as seems reasonable while monitoring heart rate and the electrocardiogram (4).

An antihistaminic (chlorphenamine) should be administered as a secondary measure. Caution is needed to avoid "drug induced" hypotension: administer either by slow intravenous injection or by intramuscular injection. Its use may be helpful and is unlikely to be harmful. The dose for children and adults is determined by age as follows:

	> 12 years :	10 - 20 mg IM
	6 - 12 years:	5 - 10 mg IM
	1 - 6 years:	2.5 - 5 mg IM

Hydrocortisone should be administered after severe attacks to help avert late sequelae. This is of particular importance for asthmatics (who are at increased risk of severe or fatal anaphylaxis) if they have been treated with corticosteroids previously. The dose of hydrocortisone should be given by slow intravenous or intramuscular injection - care being taken to avoid inducing further hypotension. The dose for adults and children is determined by age as follows:

	> 12 years :	100 to 500 mg IM
	6 - 12 years:	100 mg IM
	1 - 6 years:	50 mg IM

If severe hypotension does not respond rapidly to drug treatment, fluid should be infused. A crystalloid may be safer than a colloid. A rapid infusion of 1-2 L may be needed. Children should receive 20 mls/kg rapidly, followed by another similar dose if there is no clinical response.

Patients with even moderately severe attacks should be warned of the possibility of an early recurrence of symptoms and in some circumstances should be kept under observation for up to 8 -24 hours.

In our case though the diagnosis was not clear to start with, we managed with standard resuscitation guidelines. We also looked at other possibilities of cardiac arrest under anaesthesia and managed on those lines.

References:

1. Keenan RL and Boyan CP. Decreasing frequency of anesthetic cardiac arrests. J Clin Anesth 1991; 3:354–7

2. British Journal of Anaesthesia 2006 96(5):569-575; doi:10.1093/bja/ael065

3. Australian Anaesthesia website- http://www.usyd.edu.au/anaes/austan/anaphylaxis.html#investigation

4. Resuscitation Council UK guidelines.

.

A case report of prolonged laryngeal oedema after posterior cranial fossa surgery

Sangram Patil¹

Madhu Gowda²

1. Specialist Registrar in Anaesthetics, Morriston Hospital Swansea, SA6

6PU, UK.

2. SHO in ITU, Morriston Hospital Swansea, SA6 6PU, UK.

Case report:

A 62 yrs lady was transferred to our neurosurgical unit to assess and investigate the cause for hydrocephalus. Her presenting complains were difficulty in swallowing and walking for last 3 months, worsening paraesthesia & numbness of left upper limb and worsening memory for last few weeks. She was non-smoker.

Her background history was hypertension, hypothyroidism, hiatus hernia, basal cell carcinoma of face and duodenal perforation operated in the past. Her preoperative examination showed normal higher functions, cranial nerves, unsteady gait and reduced left upper limb power. CT scan of head showed distortion of ventricles, suspicion of posterior fossa mass. Her thyroid functions were normal.

She underwent excision of ependymoma 4^th ventricle, resection of tonsils and insertion of ventricular drain. The operation was performed in prone position and lasted 6 hours. She was extubated at the end of operation and transferred to neuro ICU. On neuro ICU she developed increasing stridor and needed reintubation.

Laryngoscopy showed grade 1 view and laryngeal inlet was swollen & appeared crescent shaped. Only size 6.5 cm endotracheal tube could pass through the cords due to laryngeal oedema. She subsequently developed chest infection. On ventilator she was moving all 4 limbs and obeying commands. CT scan of head showed expected postoperative findings.

On day 8 she was reviewed in view for extubation. On deflation of endotracheal tube cuff there was good leak around the tube and she ventilated well spontaneously. Fibre optic scopy showed slightly oedematous vocal cords. On extubation patient developed stridor, difficulty in speaking and needed intubation again (awake fibre optic nasal intubation).

She underwent elective tracheostomy in theatre. Meanwhile, she became drowsier and developed weakness in proximal muscles. CT scan head showed chronic SDH of increasing size.

She subsequently settled and could breathe spontaneously with tracheostomy mask with speaking valve and later minitrach.

Neurological review after 3 weeks of admission showed left facial weakness with nystagmus, weakness in the distribution of 9^th & 10^th cranial nerves. She had a husky voice with evidence of incomplete closure of vocal cords.

ENT surgeon opined that her soft palate on left was normal and on right the function was diminished. Left vocal cord was immobile, arytenoid cartilage displaced anteromedially. Left cord was in paramedian position and there was incomplete right cord compensation.

The patient was discharged to rehabilitation ward after a month of ICU stay. The issues at discharge were bulbar palsy, left upper limb weakness and unsteady gait. Minitracheostomy was removed before discharge.

Discussion:

Prone position in posterior fossa surgery requires substantial flexion of neck to facilitate surgical access. This causes reduction of anterior-posterior dimension of hypopharynx, compression ischemia of base of tongue, soft palate, posterior wall of pharynx (against ETT or oral airway). The consequence of this can be post-extubation airway obstruction of rapid onset as a result of macroglossia caused by accumulation of oedema. Macroglossia after prone position surgery has been well described.¹ An unusual case of massive oropharyngeal swelling and macroglossia occurring after cervical spine surgery performed on a patient in the prone position has been described.²

Posterior fossa is relatively small space; relatively little swelling can result in disorders of consciousness, respiratory drive and cardio-motor function. Irritation and injury of posterior fossa structures that may have occurred during surgery need to be taken into account when planning extubation and postoperative care. Procedures involving dissection on the floor of 4^th ventricle entail possibility of injury to cranial nerve nuclei or postoperative swelling. Injury of 9^th, 10^th & 12^th cranial nerves can result in loss of control/patency of upper airway

The intubation trauma can lead to tears in mucosa of larynx, trachea, and arytenoid cartilage dislocation causing hoarseness. Pressure effects due to shape of ETT may exert substantial pressure on arytenoid cartilages. Pressure effects of cuff can cause nerve injury due to pressure on braches of recurrent laryngeal nerve.

Post intubation laryngeal oedema is commonly symptomatic in children as their small airway size is more severely reduced by oedema and is usually subglottic. The possible causes could be large ETT, trauma from laryngoscopy and intubation, excessive neck manipulation during intubation and surgery, coughing and bucking on tube and recent upper respiratory tract infection.

Long-term intubation can cause trauma, ulceration, healing with fibrotic scar tissue causing stenosis, granuloma and web formation. The incidence of laryngeal complications after prolonged intubation is between 4% and 13%. Benjamin has described several stages of injury and the resultant chronic laryngeal changes that may be seen after prolonged intubation.³ The earliest of these changes are non-specific hyperaemia and oedema due to mucosal irritation. Oedema within the submucosa in the subglottis at the level of the cricoid may increase slowly leading to delayed airway obstruction hours after the removal of the endotracheal tube.

V Narayan et al has reported a case of unilateral tongue, face and neck swelling after prolonged operation in lateral position with extreme neck flexion.⁴

We think the causes for prolonged laryngeal oedema in our case were prolonged posterior cranial fossa surgery and neck flexion in prone position.

Conclusion:

From the literature and our case report we conclude that following factors need to be kept in mind for post-operative laryngeal oedema -

Prolonged surgery

Prone position

Posterior cranial fossa surgery including resection of cerebellar tonsils

Hypothyroidism

Traumatic intubation

Extreme neck positioning during operation

Anaesthetist & surgeon need to interact to make decisions regarding whether extubation is appropriate and the location for postoperative observation.

References:

1. McAllister RG. Macroglossia: a positioning complication. Anesthesiology 1974; 40:199–200.

2. Sinha, Ajay; Agarwal, Anil; Gaur, Atul; Pandey, Chandra Kant. Journal of Neurosurgical Anesthesiology. 13(3):237-239, July 2001.

3. Benjamin B. Laryngeal trauma from intubation: endoscopic evaluation and classification. In: Cummings CW, et al., ed., Otolaryngology-Head&Neck Surgery, 3^rd ed., St. Louis: Mosby, 1998:2013-35.

4. Bhadri Narayan, MD and G. S. Umamaheswara Rao, MD. Unilateral Facial and Neck Swelling After Infratentorial Surgery in the Lateral Position. Anesth Analg 1999;89:1290

Severe Sepsis of Unknown Cause

Sangram Patil1, Indrani Banerjee2
1. Specialist registrar in Anaesthetics, Morriston Hospital Swansea, SA6 6PU, UK.
2. SHO in Anaesthetics, Ysbyty Gwynedd, Bangor LL57 2PH, UK.

Case summary

37 yr female presented with initial complaints of feeling unwell, poor appetite and abdominal pain. She was referred to a medical unit by her psychiatrist a week before and was diagnosed to have gastritis after upper GI endoscopy. While on ward her BP was recorded to be 75/ 50 mmHg at one point. She was discharged from hospital after couple of days of medical therapy for gastritis.

This time she rapidly developed acute renal failure due to dehydration/sepsis. Due to falling consciousness levels and respiratory failure she was admitted on the ITU. Her clinical picture was not clear. To rule out encephalitis/ meningitis lumbar puncture was performed on admission to ITU. She was intubated and ventilated for deteriorating general condition and sepsis. LiDCO monitoring was initiated.

She met criteria for severe sepsis-
High temperature 40oC
Heart rate 177/ min
Hypotension Systolic BP 45 mm Hg
Hypoxemia SaO2 85 %
Acute oliguria

Her investigations showed-
CXR Clear
CT scan head Normal
Lumbar puncture Unremarkable
Gynaecology referral Normal

‘Sepsis Care Bundle’ was initiated which included-
Early diagnosis and treatment
Hydrocortisone
Glycaemic control
Activated Protein C
Limit ventilation pressures

There is an ongoing research in our hospital which includes serum sampling for cortisol levels taken prior to commencing hydrocortisone administration for every patient with sepsis. This patient was now appearing to be a case of Addison’s disease (cortisol level < 28nmol/L) with MODS and sepsis. She was started on infusion of hydrocortisone 10 mg/ hr. Haemofiltration was instituted to correct acidosis and renal failure. Activated protein C was administered as she fulfilled criterions for it.
CT scan of chest, abdomen and pelvis was normal. Rheumatological screening for organ-specific & systemic auto antibodies screen was negative.

She responded to initial aggressive measures and showed slow clinical improvement, complicated by ARDS, tracheostomy and prolonged ventilatory wean. Cortisol levels during recovery were 741 nmol/ L and depot synacthen test showed no response (proven Addison’s disease now). Hydrocortisone was replaced gradually by 30 mg/ d oral prednisolone. Fludrocortisone was added daily 100 mcg orally and patient was discharged home after few days of ward stay.

Four weeks post discharge she was seen in out patient clinic by endocrinologist, where she complained of lethargy and tiredness. She was put on hydrocortisone 25 mg OD, fludrocortisone 100 mcg OD. Her cortisol/ ACTH day profile showed flat response.

She is now under care of endocrinologist being treated for Addison’s disease.


Discussion

Addison’s disease:

“General languor and debility, remarkable feebleness of the heart’s actions, irritability of the stomach, and a peculiar change in the colour of the skin” – Addison. Primary Addison’s disease is relatively rare. There needs to be 90% functional destruction of adrenals before symptoms of this condition.
Lab findings of Addison’s disease are:
Low urinary cortisol
Low basal cortisol and aldosterone, subnormal response to ACTH
↑ Ca++, ↑ K+, ↓ Na+, ↓ Cl-, ↓ HCO3-.

Short synacthen test:

Indications:
Diagnosis of primary adrenal insufficiency
Assessment of ACTH reserve

Contraindications:
This test is unreliable within 6 weeks of pituitary surgery.
If not urgent female patients should avoid oral HRT or oral contraceptives for 6 weeks. In patients with allergic disorders e.g. asthma.

Procedure:
Patient needs to be non-fasting. If on hydrocortisone, omit previous evening and next morning doses. Take blood at 0900hr for cortisol estimation. Give intramuscular tetracosactide 250µg. Take blood samples at 30 and 60 minutes post synacthen for cortisol estimation.


Interpretation guidelines:
Serum cortisol should rise to >550mmol/L at 30 minutes.
Failure indicates adrenal insufficiency, whether primary or secondary.

NB Unreliable test within 6 weeks of pituitary surgery


Conclusion

Opinion on the value of the short synacthen test is equivocal.1-3
Our patient had cortisol levels done which led to detection of Addison’s disease early in her presentation. Should every patient admitted to ITU with severe sepsis have baseline cortisol estimation? Current evidence is conflicting. More research is needed in this field to provide definitive guidelines.


References

Loisa P Uusaro A Ruokonen E. A single adrenocorticotropic hormone stimulation test does not reveal adrenal insufficiency in septic shock. Anaesthesia & Analgesia. 101(6):1792-8, 2005 Dec.
Ligtenberg JJ, Zijlstra JG. The relative adrenal insufficiency syndrome revisited: which patients will benefit from low-dose steroids? Current Opinion in Critical Care. 10(6):456-60. 2004 Dec
Bourne RS, Webber SJ, Hutchinson SP. Adrenal axis testing and corticosteroid replacement therapy in septic shock patients – local and national perspectives. Anaesthesia. 58: 571-596. 2003

Intensive care management of a patient of idiopathic liver cirrhosis who presented with severe gastrointestinal bleeding

Introduction:

Gastrointestinal bleeding:

GI tract is highly vascular.

Major bleeds are threat to survival.

GI bleed may be primary pathology or complication of other disease process.

Upper GI bleeds are larger and more rapid.

Common cause for or complication of ITU admission.

Case summary:

A seventy two year old lady was admitted to intensive care unit following massive haematemesis and malaena. Her background history was as follows-

Hypothyroidism on thyroxin replacement, severe rheumatoid arthritis, idiopathic liver cirrhosis with oesophageal varices for which she had received scerotherapy in the past. She had had admission to intensive care unit for long period in past for decompasated liver failure.

This time she had 4 episodes of large volume haematemesis associated with malaena. She remained haemodynamically stable to start with. She was transferred to HDU to observe her closely. She was started on omeprazole intravenous regimen and terlipressin. Her coagulation remained stable.

While on HDU, she had 4 episodes of haematemesis in quick succession making her haemodynamically unstable and tired. In view of protecting her airway and putting Sengstaken tube for control of variceal bleed decision was taken to electively ventilate her. After endotracheal intubation Sengstaken tube was passed using laryngoscope to guide the insertion. Gastric balloon was inflated with 350 ml air and oesophageal balloon with 75 ml air. This stopped further bleeding from upper GI tract.

Meanwhile, she needed blood transfusions to maintain her haemoglobin around 10g/dl. As the bleeding looked settled, the oesophageal balloon was deflated and sengstaken tube was removed later after deflating stomach balloon.

The medical team carried out OGD scopy while patient was still intubated. There was no evidence of oesophageal bleed, but the gastric fundus showed varices with clot attached to them. No intervention was done as disturbing the clot might have caused more bleeding. The plan was made for repeat scopy later for injection therapy for fundal varices.

The patient was successfully extubated and further care was handed over to gastroenterology team.


Discussion:

Cirrhosis can be caused by a prolonged or intense contact of liver tissue with various substances including excess alcohol, damage by some drugs, poisons such as arsenic, hepatitis, NASH, inherited diseases such as haemochromatosis, and Wilson’s disease. Some times the cause of cirrhosis is not known; the disease is said to be idiopathic.

Portal hypertension is hypertension (high blood pressure) in the portal vein and its branches. It is often defined as a portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins) of 12 mm Hg or greater.

Consequences of portal hypertension are caused by blood being forced down the alternate channels by the increased resistance to flow through the portal system. They include:

· Ascites

• Hepatic encephalopathy
• Increased risk of spontaneous bacterial peritonitis
• Increased risk of hepatorenal syndrome
• Splenomegaly with consequent sequestration therein of red blood cells, white blood cells, and platelets, together leading to mild pancytopenia
• Portacaval anastomoses (Esophageal varices, hemorrhoids, caput medusae), with esophageal varices posing an ongoing risk of life-threatening hemorrhage.

Medical management:

Treatment with a non-selective beta blocker is often commenced once portal hypertension has been diagnosed, and almost always if there has already been bleeding from esophageal varices (either propranolol or nadolol). Addition of a nitrate, such as isosorbide mononitrate, to the beta blocker is more effective than using beta blockers alone and may be the preferred regimen in those people with portal hypertension who have already experienced variceal bleeding. In acute or severe complications of the hypertension, such as bleeding varices, intravenous octreotide (a somatostatin analogue) or intravenous terlipressin (an antidiuretic hormone analogue) is commenced to decrease the portal pressure.

Emergency management of bleeding varices:

Fluid Resuscitation – blood and colloids

Correct coagulopathy

Stop Haemorrhage - tamponade

A Sengstaken-Blakemore tube is generally used only in emergencies where bleeding from presumed varices is impossible to control by administration of medication. It may be difficult to position, particularly in an unwell patient, and may inadvertently be inserted in the trachea, hence endotracheal intubation before the procedure is strongly advised to secure the airway. It is a temporary measure: ulceration and rupture of the esophagus and stomach are recognized complications (1). Also, it can be misplaced into trachea causing massive lung damage (2).

Percutaneous interventions:

Transjugular intrahepatic portosystemic shunting is the creation of a connection between the portal and the venous system. As the pressure over the venous system is lower than over a hypertensive portal system, this would decrease the pressure over the portal system and a decreased risk of complications.

Surgical interventions:

· Distal splenorenal shunt

• Liver transplant

The most definitive treatment of portal hypertension is a liver transplant.

Our patient was managed on standard therapy and responded well.

References:

1. Bauer JJ, Kreel I, Kark AE. The use of the Sengstaken-Blakemore tube for immediate control of bleeding esophageal varices. Ann Surg 1974;179:273-7.

2. Chien JY, Yu CJ (2005). "Images in clinical medicine. Malposition of a Sengstaken-Blakemore tube". N. Engl. J. Med. 352 (8): e7.

Case report

A case of snake bite

Sangram Patil¹

Madhu Gowda²

1. Specialist registrar in Anaesthetics, Morriston Hospital Swansea, SA6 6PU, UK.

2. SHO in ITU, Morriston Hospital Swansea, SA6 6PU, UK.

Introduction

Snake bite though very rare in UK, is a very common life-threatening condition in many tropical countries. Snake bite causes 3-5 million victims/yr with nearly 50,000 deaths & staggering 4,00,000 amputations world-wide. About 40% bites by venomous snakes don’t produce signs of envenoming. As it is difficult to predict which bites produce symptoms or clinical outcome, all victims should be treated and observed under medical care immediately. Here we report a case of snake bite brought to our hospital for emergency treatment.

Case summary

A 54years lady with adder snake bite was brought to casualty by air ambulance.

She had bite mark to her right big toe. At the scene she squeezed the toe immediately. She had a vomiting episode and developed confusion subsequently.

On the way to hospital, in an ambulance, she developed typical anaphylactic reaction- she became hypotensive (BP 76/54 mmHg), agitated with pain in affected big toe and foot.

Paramedics gave her adrenaline 0.5 mg intramuscularly and pushed intravenous fluids (2 litres of crystalloid + colloids) to which she responded well.

On arrival in emergency department she was conscious, oriented (GCS 13) and was phonating well. She had a difficulty in swallowing, complained of pain right foot, abdomen and change in voice. She vomited immediately on arrival to casualty.

Her clinical examination revealed-

Tongue swollen

The affected site: cellulitic reaction, puncture wound, splint in-situ. Her cardiovascular and respiratory parameters were stable.

Treatment in A & E-

Humidified oxygen with face mask

Intravenous fluids

Piriton & Hydrocortisone

Augmentin to cover the snake bite site

Tetanus injection

Antivenom- as per protocol.

Morphine for pain relief.

She was continuously monitored. After couple of hours she improved clinically. She became completely alert (GCS: 15/15) and was haemdynamically stable

Tongue swelling reduced and her voice improved. Foot pain got better.

Observations at 24 hours were-

Leg swelling worsened

She developed right groin lymphadenopathy

The affected leg became oedematous and hot

Her coagulation was slightly deranged with prothrombin time 19, APTT 45 seconds.

Snake bite specialists in Liverpool were contacted for further treatment. The advised that there was no evidence for steroid and asked to watch for necrotic changes in foot.

At 48 hours-

Her swelling improved and she became symptomatically better. Her coagulation parameters returned to normal.

At 72 hours-

She was very comfortable and independent and was discharged home with advice to watch for swelling, redness or any unusual symptoms.

Discussion:

Amount of venom injected via the bite is highly variable. It depends on the length of time since the snake last ate and also its aggression. The clinical effects of snake bite will depend on the type of snake involved. In our case the lady knew the type of snake well. The relatives/friends may bring the snake with them to hospital.

Snake venom is complex mixture of proteins & small polypeptides with enzymatic activities. Snake venom can be neurotoxic, haematoxic or myotoxic, usually a combination of these.

Our patient had a combination of signs and symptoms. The usual clinical picture is as follows.

The signs & symptoms of envenomation:

Vomiting

Diarrhoea

Abdominal pain

Angioedema and shock

Confusion and/or drowsiness

Loss of consciousness

Unrecordable pulse and/or BP

Swelling and discoloration of the whole of the affected limb and trunk

Lymphadenopathy

Non-specific ECG changes, heart block, cardiac arrhythmias

Coagulopathy

Coma & Seizures

Pulmonary edema, adult respiratory distress syndrome (ARDS)

Acute pancreatitis & renal failure

The initial first aid received was accurate and in time. She also received advanced treatment for allergic manifestations on the way to hospital. This could have been resulted in milder course later on. The guidelines for management of snake bite are-

Reassure

Immobilise the bitten area (minimises venous spread)

Identify the snake

Firm bandage to occlude lymphatic drainage

Unhelpful things are–

Tourniquets – doesn’t prevent venom spread & often applied incorrectly

Incision @ bite site & attempt to suck out

Hospital Management-

Observation for 12 – 24 hrs

Symptomatic treatment for - pain & vomiting

Anti-tetanus

Timely administration of species specific antivenin

Rule of h/o allergy – intradermal sensitivity testing

Coagulopathy/thrombocytopenia/DIC: FFP, cryoprecipitate & platelets ay be indicated.

In our case clotting abnormalities were self-limiting and did not need any treatment.

She did not develop excessive swelling of her affected limb, rhabdomyolysis or compartment syndrome.

Because of cardiovascular instability during transfer and increasing swelling she received antivenin. The antivenin is indicated in following situations-

Cardiogenic Shock

Spontaneous systemic bleeding

Incoagulable blood

Neurotoxicity

Haematuria

Evidence of haemolysis/rhabdomyolysis

Rapidly progressive extensive swelling

Bites on digits by snakes with known necrotic venoms


Most commonly seen snake in UK is European Adder (Viperidae family). Antivenom for this snake is Antivenin Vipera tab (European Viper antivenom).

Prevention is better than cure. Awareness & avoidance of the habitat of snakes may help to reduce the incidence of snake bite.

References:

·Davidson’s principle & practice of Medicine – 20^th edition

·Sprivulis P, Jelinek G Toxicology - Snakebite. In: Cameron et al.(eds). Textbook of Adult Emergency Medicine 2nd Ed. Churchill Livingstone, Edinburgh pp. 881-884

·Stewart CJ; Snake bite in Australia: first aid and envenomation management.;Accid Emerg Nurs 2003 Apr;11(2):106-11.[abstract]

·Harborne DJ; Emergency treatment of adder bites: case reports and literature review.;Arch Emerg Med 1993 Sep;10(3):239-43.[abstract]

·TOXBASE. Poisons information site.

·Sutherland S, Tibballs J. First Aid for Bites and Stings. In Australian Animal Toxins 2nd Ed. OUP 2001. pp28-47

·Thomas PP, Jacob J. Randomized trial of antivenom in snake envenomation with prolonged clotting time. Brit Med J 1985;291:177-178.

·Warrel DA, Venoms, toxins and poisons of animals and plants. In: Wealtherall DJ, Ledingham JGG, Warrell DA (eds) Oxford Textbook of Medicine. 3nd ed. Vol 1, Oxford, Oxford University Press. 1996.