Albumin for Resuscitation in Critical Illness

 

A 50-year-old man was brought to the emergency department. He had sustained a burn affecting 55% of his total body surface area and a significant inhalational injury.  In the emergency department he was intubated and ventilated, central venous, arterial and urinary catheters were placed and resuscitation begun using the Parkland formula.

He was transferred to burns intensive care.  Fluid resuscitation was continued using Hartmann’s solution.  A bronchoscopy was performed; 1.26% sodium bicarbonate was used for lavage.  He became increasingly tachycardic and hypotensive.  He was oliguric.  His haematocrit was 0.45.  Fluid status was difficult to assess clinically; he felt warm to touch.  An oesophageal Doppler probe was sited which demonstrated low stroke volume and corrected flow time.  His Doppler parameters improved with each 250ml bolus of Hartmann’s solution but the effect was short lived.  Noradrenaline and then adrenaline infusions were used in an attempt to maintain blood pressure.  After a significant volume of crystalloid had been given, approximately 12 hours after the time of injury, 4.5% human albumin solution was requested.  This seemed to have a more prolonged effect than Hartmann’s solution.  Over the next 12 hours the patient’s haemodynamic status stabilised and he was able to undergo initial surgical management of his burn 36 hours after presentation.

What is the evidence for the use of human albumin solution for fluid resuscitation in critically ill patients.Read More »

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Management of Variceal Bleeding

A 50 year-old man with a history of alcoholism attended to the emergency department having been found at home comatose.

He had a reduced Glasgow coma score on admission and was vomiting blood. He was not protecting his airway and was tachypnoeic, tachycardic and had a reduced systolic blood pressure. His oxygen saturations were low and there were coarse crackles on his chest. Old notes showed that on previous endoscopy oesophageal and gastric varices were found. He was cachectic with hepatosplenomegaly but no signs of ascites.. He was rumoured to be abstinent from alcohol and had been previously well up to one day ago when he was last seen. There was some report that he had been behaving oddly over the last 5 days though.

 

Supplemental oxygen was provided and the decision to intubate was made. An initial attempt to insert a Sengstaken-blakemore tube was abandoned until the patient was intubated using a rapid sequence intubation technique. The gastric balloon was inflated and put under tension. Blood tests showed a reduced haemoglobin level but no clotting abnormality. Transfusion of packed red cells was made.

Medical therapy included beginning a course of prophylactic antibiotics. Terlipressin was started at 2mg intravenously four times daily. He was also started on high dose proton pump inhibitors, lactulose and thiamine supplements.

The gastric balloon was left inflated for 10 hours and as there was no haemodynamic sign of further bleeding was then deflated. Oesophagogastrocopy the next morning on the intensive care unit showed only grade 1 varices with no recent stigmata of bleeding and some mild gastric erosions.

He continued to be haemodynamically stable and sedation was weaned. He did not wake up as expected on sedation hold and his ammonia level was found to be raised. Over the course of the next 2 days he improved and was extubated successfully and discharged to the ward.

Describe the management of variceal bleeding.

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Vasopressin Versus Vasopressin Analogues in Septic Shock

A 52 year old female was admitted to the ICU with septic shock secondary to cholangitis. She had liver cirrhosis secondary to alcoholic liver disease, although she had been abstinent since an admission with acute alcoholic hepatitis  2 years previously. She had recently entered the assessment pathway for orthotopic liver transplantation.

She presented to the Emergency Department with a short history of fever and confusion and falls. She was pyrexial, tachycardic and hypotensive. Her inflammatory markers were elevated and her liver enzyme profile suggested cholestasis. There were no other localising features on examination or preliminary investigation.

She was commenced in the ED on broad-spectrum antibiotic therapy (piperacillin-tazobactam) and fluid resuscitation consisting of Hartmann’s solution and 4% human albumin solution. Her blood pressure remained labile throughout the early part of her admission. She fulfilled the criteria for septic shock with evidence of evolving multi-organ dysfunction.

 

The patient received early, aggressive multi-organ support. Tracheal intubation and pressure-controlled ventilation were instituted due to grade III/ IV encephalopathy and a high work of breathing in response to profound metabolic acidaemia. A thorough clinical assessment of intravascular volume status was conducted, suggesting that the patient was adequately filled. Vasopressor therapy was initiated using noradrenaline to achieve a target MAP of 65mmHg. CVVHDF was commenced to control the severe acidaemia and hyperlactataemia.

The patient was vasoplegic and remained profoundly hypotensive despite rapidly escalating doses of noradrenaline and the addition of hydrocortisone. Continued assessment of intravascular status confirmed adequate filling and cardiac output monitoring using a pulse-contour analysis system confirmed a low SVRI- high cardiac output state.  Her noradrenaline requirements soon exceeded 0.4mcg/kg/min-1, at this point a vasopressin infusion was introduced at 0.03units/hr-1. This was associated with an improvement in haemodynamic indices; the target MAP was achieved and thereafter remained stable with a slow reduction in noradrenaline requirement. On day 2 the continuous vasopressin infusion was converted to terlipressin by bolus dose regime (2mg QDS).

An urgent ultrasound scan of her biliary system revealed an obstructed common bile duct which was treated by percutaneous biliary drainage. An Enterococcus was isolated from drain fluid and blood cultures within 48 hours and antibiotic therapy tailored accordingly. The patient was weaned from organ support and discharged to the hepatology unit 9 days after admission.

What is the rationale for the use of vasopressin in septic shock? Are vasopressin analogues as effective?Read More »

Propofol Infusion Syndrome

A 28-year-old man was involved in a high-speed road traffic accident suffering severe head injury (diffuse axonal injury) with bilateral haemopneumothoraces and pulmonary contusions. He was transferred intubated and ventilated to the neurointensive care unit from a district general hospital for intra-cranial pressure (ICP) monitoring.

He was initially managed with bilateral chest drains and conservative neuroprotective measures for difficult to control ICP. He was heavily sedated on propofol (300mg/hr), midazolam (30mg/hr) and fentanyl (300mcg/hr).

Over the next few days his temperature increased and he became increasingly hypoxic. He subsequently developed ECG changes and a echocardiogram showed right heart failure. A diagnosis of pulmonary embolism, which was confirmed on CTPA a few days later which showed evidence of a small PE. He was not anticoagulated due to neurosurgical concern regarding his head injury.

Over the next few days he developed renal failure requiring renal replacement therapy and acute liver failure with hypoglycaemia and lactic acidosis. He developed severe cardiovascular failure requiring multiple inotropes and pulmonary artery catheter guided therapy. Lipids were found to be elevated, with creatine kinase >50,000 and myoglobin found in the urine. Propofol infusion syndrome was diagnosed. Sedation was stopped and he started to make a recovery.

What are the clinical features of propofol infusion syndrome?

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Intra-Abdominal Hypertension

 

A 48 year old male was admitted to the ICU with rapidly evolving multi-organ dysfunction. He was in type I respiratory failure, hypotensive and had stage II acute kidney injury. He had been an inpatient recovering from a laparotomy for major urological surgery 5 days prior to his ICU admission. This was complicated by a major intraoperative haemorrhage.

The patient was commenced on treatment for presumed hospital acquired pneumonia. He was placed on mechanical ventilation and a noradrenaline infusion was commenced to maintain a mean arterial pressure of ≥65mmHg. Over the following 24 hours the patient displayed worsening lung compliance in the context of adequate oxygenation and an atracurium infusion was started. Simultaneously the patient appeared to develop an ileus and he became anuric. Repeated clinical examination revealed an increasingly distended abdomen. A CT of the abdomen and pelvis showed a large left sided retroperitoneal haematoma with evidence of pelvico-ureteric leak on the left and an associated fluid collection. The patient was taken to theatre for urgent re-laparotomy.

At the conclusion of the operation, the surgical team was unable to close the abdomen due to significant bowel oedema. They accepted a laparostomy and returned the patient to ICU with a negative pressure wound dressing in-situ. Post-operatively, there was significant improvement in lung compliance, vasopressor requirement and urine output. Enteral feeding was quickly re-established. The abdomen was closed during the same hospital admission and the patient survived-to-discharge home. At no point was this patient’s intra-abdominal pressure measured.

 

Describe the management of intra-abdominal hypertension.

Christopher Westall

Intra-abdominal hypertension (IAH)- abdominal compartment syndrome (ACS) is a well-recognised cause of morbidity and mortality in critically ill patients, rising to prominence in the 1990s with increased early survival of patients with intra-abdominal pathology requiring emergent laparotomy (principally abdominal aortic aneurysm repair and blunt trauma).1,2 IAH/ ACS may be precipitated by a range of insults local (primary IAH) and distant (secondary IAH) to the abdomen.3 The syndrome encompasses a spectrum of severity and there are a range of treatment options, though with little high quality evidence to support these.

The World Society of the Abdominal Compartment Syndrome (WSACS) consensus guidelines recommend that intra-abdominal pressure (IAP) is measured using the trans-bladder technique in any critically ill patient with an associated risk factor for IAH. The normal value for IAP is <12mmHg. IAH is then categorized by increasing pressure increments from grade I (IAP 12-15mmHg) to grade IV (>25mmHg). Abdominal compartment syndrome is defined as sustained IAP >20mmHg associated with new organ dysfunction.3

The WSACS Consensus proposes a management algorithm for IAH/ ACS that is loosely analogous to commonly encountered algorithms for managing raised intracranial pressure The abdomen is considered a fixed compartment with intra-luminal and extra-luminal volumes that can be manipulated through neutral-negative fluid balance, nasogastric and colonic decompression and percutaneous drainage of ascites/collections. In this instance, however, the compliance of the “box”, the abdominal wall, can also be manipulated by patient position, ventilatory strategy and neuromuscular blockade. Decompressive [laparotomy] therapy is reserved for algorithm failure.

The efficacy of protocolised management of IAH/ACS has never been demonstrated. A single prospective observational study suggested reduction in morbidity and mortality using algorithm based management of IAH; the authors quoted an increase in survival-to-discharge rate from 50 to 72% (p= 0.015) across 6 years with improved rates of same-admission closure. However the study was single centre, recruiting patients only after the laparostomy, with substantial selection and observer bias. Furthermore it was unclear which parts of the protocol were effective.4 While the basic principles underlying the WCASC 2013 algorithm are sensible, it must be acknowledged that proposed therapies such as resuscitation with hypertonic fluids, diuretic-driven diuresis and ultrafiltration through renal replacement therapies have no evidence to support them and have potentially serious implications for the patient.

Given that the efficacy of protocolised management of IAH/ACS is uncertain, is there then any evidence to support the measurement of IAP in every “at risk” patient, especially since the list of risk factors for IAH is so extensive that it is difficult to imagine a critically ill patient that is not at risk. This would not be without significant task-burden to critical care nursing staff, and as with any clinical index in ICU, risks morbidity from misinterpretation. There are only two small studies that have examined whether clinical examination can reliably predict intra-abdominal pressure; both small studies with significant methodological flaws and both conducted between 1996- 2000 when awareness of IAH was comparatively low. Importantly both studies compared examination to IAP measurement at pressures well below 20mmHg, where there is little evidence that specific intervention improves patient outcome, beyond highlighting that that patient is at risk of ACS.5,6

Decompressive laparotomy is recommended for the treatment of all patients with ACS refractory to medical therapy.3 In modern practice it is difficult to accurately assess the performance of this strategy in primary IAH/ACS, such is the absence of clinical equipoise. As many reviews acknowledge, the improvement in patient survival rates associated with primary laparostomy in abdominal trauma patients in the 1990s caused a fundamental paradigm shift from which it is now difficult to ethically justify alternative treatment strategies.1,2 That is to say that many patients with IAH/ ACS will now present to the ICU once decompressive laparostomy has either occurred or is imminently planned.

The benefits of decompressive laparotomy in secondary ACS are certainly less; data exists only for acute severe pancreatitis and sepsis associated with secondary peritonitis. While in both instances it must be acknowledged that laparostomy reduces IAP, like many interventions in a critically ill patient population, this does not translate into mortality benefit.7,8 As commentators note, laparostomy may often be performed because of a conceptual benefit of relook-laparotomy 48 hours later, rather than inability to close the abdomen or specific concerns regarding ACS.2 Indeed, regarding secondary peritonitis, there is good evidence that primary closure with on-demand re-laparotomy is non-inferior to laparostomy and planned re-laparotomy, and is associated with fewer surgeries and lower healthcare costs.9 This strategy is now [weakly] endorsed by the WCACS.3

One point that is widely agreed upon is the management of laparostomy. It appears universally agreed that negative pressure wound therapy (NPWT, i.e. “vac dressings”), with or without a form of dynamic retention system, is superior to previously popular methods such as bioprosthetic mesh and Bogota bag. The largest systematic review on the subject suggests that NPWT is associated with improved rates of primary delayed fascial closure (57.8%, 95% CI 50.8- 64.7) and mortality (22.3%, 95% CI 17.5- 27.5) with lower rates of entero-atmospheric fistulation (7.0%, 95% CI 5.0- 9.3) and abscess formation (4.2%, 95% CI 2.3- 6.9).10 This systematic review heavily influenced the most recent NICE review on the topic leading to endorsement of NPWT in clinical guideline IPG467, “Negative pressure wound therapy for the open abdomen” (2013).


Conclusion

The measurement of IAP in all at-risk critically ill patients is probably unnecessary and burdensome in resource terms. Critical care practitioners should have a low index of suspicion for ACS in their patients; if this develops then decompressive laparotomy is the treatment of choice (unless there is a large extra-luminal collection amenable to urgent drainage), particularly since modern laparostomy management appears to be associated with an increasingly low complication rate, if the abdomen cannot be closed.

The consensus guidelines for IAH/ACS remind us that attention to detail; such as ensuring that enteral nutrition is succeeding, that bowel care is optimal and that fluid balance is tightly controlled, may prevent numerous serious ICU-associated syndromes from ever developing.


References

1. Balogh ZJ, Lumsdaine W, Moore EE, Moore FA. Postinjury abdominal compartment syndrome: from recognition to prevention. Lancet,  2014; 384:1466-75

2. Leppaniemi AK. Laparostomy: why and when? Critical Care 2010; 14: 216. DOI: 10.1186/cc8857

3. Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain MLNG, De Keulenaer B, Duchesne J, Bjorck M, Leppaniemi A, Ejike JC, Sugrue M, et al.  Intra-abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med, 2013; 39:1190-1206

4. Cheatham ML, Safcsak KRN. Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Crit Care Med,  2010; 38:402-407

5. Kirkpatrick AW, Brenneman FD, McLean RF, Rapanos T, Boulanger BR. Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? Can J Surg, 2000:43:207-11

6. Sugrue M, Bauman A, Jones F, Bishop G, Flabouris A, Parr M, Stewart A, Hillman K, Deane SA. Clinical examination is an inaccurate predictor of intra-abdominal pressure. World J Surg, 2002; 26:1428-31

7. Mentula P, Hienonen P, Kemppainen E, Puolakkainen P, Leppaniemi A. Surgical decompression for abdominal compartment syndrome in severe acute pancreatitis. Arch Surg, 2010; 145:764-9

8. Robledo FA, Luque-de-Leon E, Suarez R, Sanchez P, de la Fuente M, Vargas A, Mier J. Open versus closed management of the abdomen in the surgical treatment of severe secondary peritonitis: a randomized clinical trial. Surg Infect (Larchmt), 2007; 8:63–72

9. van Ruler O, Mahler CW, Boer KR, Reuland EA, Gooszen HG, Opmeer BC, de Graaf PW, Lamme B, Gerhards MF, Steller EP, van Till JW, et al. Comparison of on-demand vs planned relaparotomy strategy in patients with severe peritonitis: a randomized trial. JAMA, 2007; 298:865-73

10. Quyn AJ, Johnston C, Hall D, Chambers A, Arapova N, Ogston S, Amin AI. The open abdomen and temporary abdominal closure systems- historical evolution and systematic review. Colorectal Dis, 2012; 14: e429–38

 

Adjunctive Therapies in Bacterial Meningitis

 

A 42 year old female with type 2 diabetes presented to hospital with fevers, malaise and headache. She had become unwell 7 days earlier with coryzal symptoms, feverishness, and cough with green sputum. On examination she was unwell and intermittently drowsy but gas exchange was adequate and she was haemodynamically stable with lactate 1.5 units. Temperature was 39.6oC and glucose was 15.8 units. Chest x-ray showed bibasal consolidation. CRP was 35 units and white cell count was 12.9. She received ceftriaxone 2 g, clarithromycin 500 mg, intravenous crystalloid 1000 mL and an insulin sliding scale.

One hour after admission the patient deteriorated with GCS 6 and non-purposeful shaking movements of the right arm and leg, which resolved with diazepam 5 mg intravenously. Her airway became partially obstructed despite nasopharyngeal and oral airways and she was urgently intubated. Aciclovir 900 mg was given and the patient was transferred to the ICU.

CT head showed no abnormality. A lumbar puncture revealed turbid yellow-tinged cerebrospinal fluid (CSF). Dexamethasone 10 mg was given. A phenytoin infusion was started. Sedation was maintained with propofol and fentanyl.

The CSF showed Gram positive cocci and a white cell count of 1274 units with neutrophils 1248 units. CSF glucose was 0.3 units and protein was 5.5 g. Ceftriaxone twice daily and dexamethasone four times daily were continued and acyclovir was discontinued. Blood cultures and CSF both grew Streptococcus pneumoniae. Viral PCR was negative. After 48 hours the patient was extubated and then discharged to the ward without any neurological deficit. She went home 5 days after admission. Ceftriaxone was given for a total of 14 days, facilitated by the outpatient parenteral antibiotic therapy team. She was advised not to drive for 6 months.

What adjunctive therapies, if any, are effective in the treatment of bacterial meningitis?Read More »

Advance Decisions in Critical Care

 

An 85 year old man with good pre-morbid function was admitted to the ICU following emergency laparotomy for a ischaemic perforation of small bowel. He had undergone a small bowel resection and primary anastomosis. Preoperatively, the patient had been delirious and unable to consent for surgery, assent was granted by his wife.

Postoperatively, the patient required mechanical ventilation, vasopressor support and renal replacement on admission. He stabilised by day 5, but remained mechanically ventilated. On day 5 of admission, during a discussion between the surgeon and the patient’s wife, the wife admitted regret that she had not had “better” discussions with the surgeons pre-operatively and raised doubts as to whether the patient would have wanted such treatment. Following those discussions between the wife and surgical team, limitations on care were placed; renal replacement therapies would not be restarted and vasopressor support would not be escalated beyond the existing level. A DNR order was implemented. On day 10, during discussion with the duty ICU consultant, it emerged that the patient had a written advance decision refusing “aggressive medical treatment”.

 

The patient continued to improve but could not be weaned from ventilation. A percutaneous tracheostomy was sited on day 10. On day 15 he was liberated from mechanical ventilation and able to use a speaking valve. He had regained mental capacity sufficient to discuss his care and wished to continue given the progress he had made. It was agreed that he would not be mechanically ventilated in the event of deterioration and the existing DNR order was confirmed. Subsequently, it became apparent that the small bowel anastomosis was leaking; it was agreed that treatment would be non-operative.

In total the patient was treated on ICU for 20 days before he was placed on an end of life pathway and died.

 

What are the implications of Advance Decisions on Intensive Care?Read More »

Thrombolysis and Intermediate-Risk Pulmonary Embolism

 

A 40 year old woman was admitted to the emergency department (ED) after a syncopal episode. On admission she was in acute respiratory distress and described a two day history of sudden onset breathlessness. She had no previous medical history. Her only regular medication was the oral contraceptive pill. She had had a recent flu-like illness and been less active than usual. On arrival she had a respiratory rate of 30 breaths/minute with accessory muscle use. An ABG on 15L/min oxygen via non-rebreathe mask showed type I respiratory failure (PO2 8.4kPa). She was tachycardic (120bpm) and blood pressure was 98/50. Chest x-ray and bloods were unremarkable although her ECG revealed a sinus tachycardia with right axis deviation, Q waves and inverted T waves in lead III.

The patient had a bedside echocardiogram that revealed a severely dilated right ventricle with poor tricuspid annulus planar systolic excursion (TAPSE). A presumed diagnosis of a pulmonary embolism (PE) was made. Thrombolytic therapy was considered but rejected at this point, in view of the haemodynamic stability. The patient was commenced on enoxaparin at a dose of 1.5mg/kg.

CT pulmonary angiography confirmed the presence of bilateral pulmonary emboli. On return from CT the patient was sat up briefly at which time she became cyanotic and had a brief self-terminating seizure. During this time her blood pressure was not recordable, and significant hypotension secondary to obstructive shock was assumed to be the cause. At this point it was decided to proceed with thrombolysis. The patient was transferred to the Intensive Care Unit, made a rapid recovery without the need for vasopressors or intubation and ventilation, and was discharged from hospital a few days later.

What is the evidence for intravenous thrombolysis for intermediate-risk pulmonary embolism? Read More »

Emergency Coronary Angiography After Out-of-Hospital Cardiac Arrest


 

 

A 70 year old woman suffered an out of hospital cardiac arrest whilst playing golf. She received bystander cardiopulmonary resuscitation and two shocks from an automated external defibrillator which restored spontaneous circulation. She was intubated at the scene  and arrived in the resuscitation department cardiovascularly stable, well oxygenated and unconscious in the context of propofol sedation.

There was no prodrome suggestive of a specific aetiology for the cardiac arrest but information from relatives described an ex-smoker with hypercholesterolaemia and diet controlled diabetes mellitus who had previously undergone percutaneous coronary intervention (PCI) for ischemic heart disease. She took regular aspirin, statin and beta-blocker. A post resuscitation 12 lead ECG showed sinus rhythm, left axis deviation and non-specific lateral ischaemia. Troponin was elevated above 200 ng/L.

In view of this she was loaded with dual antiplatelet therapy and underwent emergency coronary angiography which demonstrated occlusion of two small branches (OM1 and PLV) but no large vessel coronary artery occlusion to explain the cardiac arrest. The occluded vessels were not stented. Subsequent echocardiogram and cardiac MRI demonstrated old circumflex territory scar but an otherwise normal heart and ultimately it was agreed that the cause of cardiac arrest was probably ventricular arrhythmia secondary to scar.

She was ventilated for 24 hours with targeted temperature management before being woken and extubated. Although she was initially confused, her neurology improved over approximately 48 hours such that she was discharged with no apparent neurological injury. An implantable cardiac defibrillator was placed prior to discharge to prevent sudden cardiac death from any future arrhythmia.

Clinical questions:

  1. In survivors of out of hospital cardiac arrest should we proceed to early coronary angiography with a view to PCI?
  2. If so, should we apply this approach to all such patients or only a subset?
  3. If we do proceed to early coronary angiography, should this occur before or after other investigations, specifically computed tomography (CT) of the head and chest to look for intracerebral bleed and pulmonary embolism?

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Alpha-2 agonists for sedation

 

A 66 year old woman was admitted to the ICU with acute type II respiratory failure secondary to a community acquired pneumonia (CURB-65 score 4) complicating severe COPD (FEV1 40% predicted). Collateral history revealed many concerning features; the patient had a poor exercise tolerance (mMRC dyspnoea scale score 3, exercise tolerance <100m), was alcohol dependent (drinking 120 units per week) and previously had been admitted to hospital with an exacerbation of COPD requiring NIV, and treatment for acute alcohol withdrawal.

 

Mechanical ventilation was commenced using a lung-protective strategy with permissive hypercapnia. Sedation was achieved using remifentanil and propofol, targeting a Richmond Agitation Scale Score (RASS) of -2 to 0. A noradrenaline infusion was commenced to maintain a mean arterial pressure of ≥65mmHg. A neutral cumulative fluid balance was targeted. Broad-spectrum antimicrobial therapy was continued as per local antimicrobial guidelines. Intravenous B vitamins were administered and enteral feeding was established via a nasogastric tube.

In view of the patient’s comparatively poor pre-morbid function and high risk of delirium, early extubation to NIV was identified as the preferred strategy. By day 3 the patient had improved such that this became a realistic goal. In order to prevent acute alcohol withdrawal, yet use benzodiazepines sparingly to avoid associated respiratory depression, remifentanil-propofol sedation was substituted for a clonidine infusion, which was continued following extubation. Low doses of chlordiazepoxide were used as rescue therapy in accordance with Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar) scoring.

The patient progressed well, was weaned from both NIV and clonidine and was discharged from HDU to a respiratory ward on day 8. She survived to hospital discharge.

 

What role do Alpha-2 Agonists have for sedation in critical care?Read More »