Category Archives: ICU

Stuff relevant to patients on ICU

Acute Med, All Updates, ICU, Kids, Resus, Trauma

Superglue for CVCs

In resuscitation situations, the securing of vascular catheters is an important but sometimes cumbersome process, particular when sutures are required for central lines or arterial lines.

Medical grade ‘superglue’ (cyanoacrylate) can be used and this has been described in the anaesthetic literature before(1). Now, further in vitro work shows the glue does not weaken the intravenous catheter and is not associated with bacterial colonisation(2).

I think this is perfect for resuscitation lines. Just last night I used this technique to secure a femoral arterial line during a cardiac arrest resuscitation. It was great not to have to faff around with sharp suture needles during CPR and the line felt very secure after just a few seconds.

1. Tissue adhesive as an alternative to sutures for securing central venous catheters
Anaesthesia. 2007 Sep;62(9):969-70

2. Cyanoacrylate tissue adhesives – effective securement technique for intravascular catheters: in vitro testing of safety and feasibility
Anaesth Intensive Care. 2012 May;40(3):460-6

Acute Med, All Updates, ICU, PHARM, Resus

Hypothermia after long down times

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You receive a patient resuscitated from cardiac arrest to a perfusing rhythm in your emergency department. History suggests a long ‘down time’: There was a ten minute duration of ‘no-flow’ (time from collapse to the start of resuscitation attempts).
Would this make you more likely or less likely to initiate targeted temperature management (TTM) and cool the patient to the recommended 32-34 degrees?
A recent study supports the suggestion that a longer no-flow time is associated with greater odds of survival with TTM compared with no TTM, than patients with shorter no-flow times. In other words, cooling the patient is more likely to make a difference in the ‘long down time’ patient, even though the overall survival in that group is obviously less.


Aim Mild therapeutic hypothermia has shown to improve long-time survival as well as favorable functional outcome after cardiac arrest. Animal models suggest that ischemic durations beyond 8 min results in progressively worse neurologic deficits. Based on these considerations, it would be obvious that cardiac arrest survivors would benefit most from mild therapeutic hypothermia if they have reached a complete circulatory standstill of more than 8 min.

Methods In this retrospective cohort study we included cardiac arrest survivors of 18 years of age or older suffering a witnessed out-of-hospital cardiac arrest, which remain comatose after restoration of spontaneous circulation. Data were collected from 1992 to 2010. We investigated the interaction of ‘no-flow’ time on the association between post arrest mild therapeutic hypothermia and good neurological outcome. ‘No-flow’ time was categorized into time quartiles (0, 1–2, 3–8, >8 min).

Results One thousand-two-hundred patients were analyzed. Hypothermia was induced in 598 patients. In spite of showing a statistically significant improvement in favorable neurologic outcome in all patients treated with mild therapeutic hypothermia (odds ratio [OR]: 1.49; 95% confidence interval [CI]: 1.14–1.93) this effect varies with ‘no-flow’ time. The effect is significant in patients with ‘no-flow’ times of more than 2 min (OR: 2.72; CI: 1.35–5.48) with the maximum benefit in those with ‘no-flow’ times beyond 8 min (OR: 6.15; CI: 2.23–16.99).

Conclusion The beneficial effect of mild therapeutic hypothermia increases with cumulative time of complete circulatory standstill in patients with witnessed out-of-hospital cardiac arrest.

The beneficial effect of mild therapeutic hypothermia depends on the time of complete circulatory standstill in patients with cardiac arrest
Resuscitation. 2012 May;83(5):596-601

Acute Med, All Updates, ICU, Kids, PHARM, Resus, Trauma

Hyperosmolar therapy

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A great review article from the New England Journal of Medicine summaries the current knowledge base regarding the use of hypertonic saline and mannitol for raised intracranial pressure.

Hyperosmolar Therapy for Raised Intracranial Pressure 
N Engl J Med. 2012 Aug 23;367(8):746-52
Full text access is only available to New England Journal subscribers, but I’ve summarised some of the interesting bits in a short quiz you can take to test your knowledge. Just 13 True/False questions.

If you liked the quiz and want to use it at your local teaching sessions, here’s a Keynote Version and a PowerPoint Version

All Updates, ICU, PHARM, Resus

From BURP to BILP: backwards internal laryngeal pressure

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A burns patient whose tracheal tube was accidentally dislodged and ended up placed in the oesophagus on day 2 of his ICU stay continued to spontaneously ventilate and maintain saturations on a midazolam infusion. The oesophageal tube was left in during laryngoscopy (after propofol but no muscle relaxant due to anticipated difficult airway) which revealed a cormack-lehane grade 3 view. The operator’s hand which was holding a bougie rested on the oesophageal tube, which displaced it backwards. This resulted in backwards displacement of the larynx and improved the glottic view to 2b, facilitating intubation.
The discovery of this ‘backwards internal laryngeal pressure’ manoeuvre led the authors to make the recommendation that during difficult intubation an inadvertently placed oesophageal tube should be left in place to allow a BILP manouevre, but removed if it impedes the passage of the tracheal tube.
I love anything that might improve success rates of critical procedures and this one could conceivably come in handy. I can just see Minh Le Cong inventing a transoesophageal posterior laryngal retractor for under 50 bucks…
The use of “Internal Laryngeal Pressure” to improve the laryngeal view following inadvertent oesophageal intubation in a patient with difficult airway
Anaesth Intensive Care. 2012 Jul;40(4):736-7

Acute Med, All Updates, ICU, Resus

The opposite of acute kidney injury?

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Prescribing in the critically ill patient can be a challenge due to a number of factors impacting on pharmacology:

  • variable enteral absorption and interaction with enteral feed
  • less protein binding in hypoalbuminaemic states
  • extravascular volume expansion with fluid loading and capillary leak can alter the volume of distribution
  • altered hepatic metabolism of drugs
  • impaired renal excretion
  • accumulation of toxic metabolites
  • removal by renal replacement therapy
  • interaction with other drugs

There’s another factor to bear in mind, though, which has been recently highlighted in the context of antibiotic prescription: that of Augmented Renal Clearance (ARC).
Some ICU patients have supraphysiologic renal function. Several studies have demonstrated significant numbers of ICU patients with higher than normal creatinine clearance. This is thought to be due to varying combinations of the following factors:

  • Low systemic vascular resistance and increased cardiac output leading to increased renal blood flow
  • Above factors enhanced by aggressive fluid and vasoactive therapy in pursuit of haemodynamic targets
  • These lead to increase delivery of solute to the kidneys and increased clearance

This can have implications for prescribing: the serum creatinine will not identify these patients, but it is possible that ARC will result in less effective therapy for a given dose of a renally-excreted drug, for example beta-lactam antibiotics.
An editorial by critical care physician Dr Andrew Shorr highlights the inadequacy of basing prescribing recommendations on data from the ex-vivo interaction between drug and pathogen:

‘To believe that all patients will respond in the same fashion and with the same trajectory is to become handcuffed by the median response noted in clinical trials……….The central fallacy of the bug-drug approach is that it misses the key role of the host.’

Sub-therapeutic initial β-lactam concentrations in select critically ill patients: association between augmented renal clearance and low trough drug concentrations
Chest. 2011 Dec 22. [Epub ahead of print] Free Full Text
Antibiotics in the critically ill: the bug, drug, host triad
Chest. 2012 Jul 1;142(1):8-10 Free Full Text

Acute Med, All Updates, ICU, Kids, PHARM, Resus

Don't ignore the diastolic

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Most of us are pretty good at spotting hypotension and activating help or initiating therapy.
But ‘hypotension’ in many practitioners’ minds refers to a low systolic blood pressure. Who pays serious attention to the diastolic blood pressure? A low diastolic in a sick patient to me is a warning sign that their mean arterial pressure (MAP) is – or will be – low. After all, we spend about twice as long in diastole as in systole, so the diastolic pressure contributes more to the MAP than does the systolic.
A recent study showed that a low diastolic BP was one of several factors predictive of cardiac arrest on hospital wards: the most accurate predictors were maximum respiratory rate, heart rate, pulse pressure index, and minimum diastolic BP. These factors were more predictive than some of the variables included in the commonly used Early Warning Scores that trigger an emergency review.
The ‘pulse pressure index’ examined in the study is the pulse pressure divided by the systolic blood pressure (ie. [SBP-DBP]/SBP) which of course will be higher with lower diastolic blood pressures.
Importantly, the authors point out:


“In addition, our findings suggest that for many patients there is ample time prior to cardiac arrest to provide potentially life-saving interventions.”

…suggesting that there is still room for improvement in the identification and management of patients at risk for cardiac arrest, as the NCEPOD report ‘Cardiac Arrest Procedures: Time to Intervene?’ also showed.
They also recommend:


“…although systolic BP is commonly used in rapid response team activation criteria, incorporation of pulse pressure, pulse pressure index, or diastolic BP in place of systolic BP into the predictive model may be superior.”

Perhaps this may remind all of us to keep an eye on the diastolic as well as systolic BP when patients first present to us, and to include the importance of recognising diastolic hypotension in the teaching we provide our medical, paramedical and nursing students.

Predicting Cardiac Arrest on the Wards: A Nested Case-Control Study
Chest. 2012 May;141(5):1170-6 Free Full Text here
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Background: Current rapid response team activation criteria were not statistically derived using ward vital signs, and the best vital sign predictors of cardiac arrest (CA) have not been determined. In addition, it is unknown when vital signs begin to accurately detect this event prior to CA.

Methods: We conducted a nested case-control study of 88 patients experiencing CA on the wards of a university hospital between November 2008 and January 2011, matched 1:4 to 352 control subjects residing on the same ward at the same time as the case CA. Vital signs and Modified Early Warning Scores (MEWS) were compared on admission and during the 48 h preceding CA.

Results: Case patients were older (64 ± 16 years vs 58 ± 18 years; P = .002) and more likely to have had a prior ICU admission than control subjects (41% vs 24%; P = .001), but had similar admission MEWS (2.2 ± 1.3 vs 2.0 ± 1.3; P = .28). In the 48 h preceding CA, maximum MEWS was the best predictor (area under the receiver operating characteristic curve [AUC] 0.77; 95% CI, 0.71-0.82), followed by maximum respiratory rate (AUC 0.72; 95% CI, 0.65-0.78), maximum heart rate (AUC 0.68; 95% CI, 0.61-0.74), maximum pulse pressure index (AUC 0.61; 95% CI, 0.54-0.68), and minimum diastolic BP (AUC 0.60; 95% CI, 0.53-0.67). By 48 h prior to CA, the MEWS was higher in cases (P = .005), with increasing disparity leading up to the event.

Conclusions: The MEWS was significantly different between patients experiencing CA and control patients by 48 h prior to the event, but includes poor predictors of CA such as temperature and omits significant predictors such as diastolic BP and pulse pressure index.

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Acute Med, All Updates, ICU, PHARM, Resus

COPD and heart disease interactions

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Ischaemic heart disease (IHD) and chronic obstructive pulmonary disease (COPD) often affect the same patient; in fact, more than one-third of patients with angiography-proven IHD also have COPD on spirometry(1).
A recent study suggests COPD exacerbations in patients with IHD were associated with longer (5 more days) recovery times and suffered more severe breathlessness between exacerbations(2).
An accompanying editorial highlights some important points:

  • Patients admitted with COPD exacerbations are more susceptible to myocardial infarction during the admission.
  • Infective COPD exacerbations may contribute to heart failure through systemic inflammation, autonomic activation, and increased fluid in the lung. Lung infection can increase ventilation/perfusion mismatch and increased work of breathing, further straining the heart.
  • Heart failure can be very difficult to diagnose during a COPD exacerbation because cough, dyspnoea and wheeze are common to both disorders. Physical examination may not be discriminatory, and chest radiography is insensitive to milder degrees of heart failure.

The authors recommed a high index of suspicion combined with consideration of biomarkers (BNP or pro-BNP) and imaging such as echocardiography or even nuclear medicine scans, cardiac MRI, and cardiac catheterisation.
So, next time you’re managing a COPD exacerbation, ask yourself:

  • Could there be concomitant heart failure contributing to symptoms?
  • If not, is the patient at risk of cardiac events during this admission, for which we need to be vigilant?
  • Do I need to consider additional laboratory (BNP) or imaging (echo) investigations? Remember BNP may be elevated in pneumonia and other non-cardiac critical illness, although a normal BNP rules out heart failure.
  • Should I add empiric anti-failure therapy to the acute treatment regimen?
  • If there is combined COPD exacerbation and heart failure, are there any conflicting priorities in therapy (eg. the pros and cons of beta-agonists, anticholinergics, and steroids)?

1. The complex relationship between ischemic heart disease and COPD exacerbations
Chest. 2012 Apr;141(4):837-8
2. The impact of ischemic heart disease on symptoms, health status, and exacerbations in patients with COPD
Chest. 2012 Apr;141(4):851-7
[EXPAND Click to read abstract]


BACKGROUND: Comorbid ischemic heart disease (IHD) is a common and important cause of morbidity and mortality in patients with COPD. The impact of IHD on COPD in terms of a patient’s health status, exercise capacity, and symptoms is not well understood.

METHODS: We analyzed stable-state data of 386 patients from the London COPD cohort between 1995 and 2009 and prospectively collected exacerbation data in those who had completed symptom diaries for ≥ 1 year.

RESULTS: Sixty-four patients (16.6%) with IHD had significantly worse health status as measured by the St. George Respiratory Questionnaire (56.9 ± 18.5 vs 49.1 ± 19.0, P = .003), and a larger proportion of this group reported more severe breathlessness in the stable state, with a Medical Research Council dyspnea score of ≥ 4 (50.9% vs 35.1%, P = .029). In subsets of the sample, stable patients with COPD with IHD had a higher median (interquartile range [IQR]) serum N-terminal pro-brain natriuretic peptide concentration than those without IHD (38 [15, 107] pg/mL vs 12 [6, 21] pg/mL, P = .004) and a lower exercise capacity (6-min walk distance, 225 ± 89 m vs 317 ± 85 m; P = .002). COPD exacerbations were not more frequent in patients with IHD (median, 1.95 [IQR, 1.20, 3.12] vs 1.86 (IQR, 0.75, 3.96) per year; P = .294), but the median symptom recovery time was 5 days longer (17.0 [IQR, 9.8, 24.2] vs 12.0 [IQR, 8.0, 18.0]; P = .009), resulting in significantly more days per year reporting exacerbation symptoms (median, 35.4 [IQR, 13.4, 60.7] vs 22.2 [IQR, 5.7, 42.6]; P = .028). These findings were replicated in multivariate analyses allowing for age, sex, FEV(1), and exacerbation frequency where applicable.

CONCLUSIONS: Comorbid IHD is associated with worse health status, lower exercise capacity, and more dyspnea in stable patients with COPD as well as with longer exacerbations but not with an increased exacerbation frequency.

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All Updates, ICU, PHARM, Resus

Size matters when you're sick

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A nice example of a difference between elective anaesthesia and critical care practice when it comes to airway management is the selection of appropriate tracheal tube size when intubating, which is highlighted in a recent Anaesthesia article.
In recent years progressively smaller tubes have been used in anaesthesia in pursuit of decreased tracheal injury, sore throat, and hoarseness and increased ease of placement.
Patients likely to remain intubated for some time due to critical illness, however, may benefit from larger diameter tubes for the following reasons:

  • Accumulation of biofilm debris, which increases with duration of intubation – this can significantly decrease the luminal internal diameter, but is less likely to be significant with larger tubes.
  • Work of breathing during weaning: spontaneous breathing trials prior to extubation require patients to breathe through tracheal tubes. Volunteer studies have demonstrated that work of breathing increases as tube diameter decreases.
  • Bronchoscopes and suction catheters: the standard adult ICU fibreoptic bronchoscope has a diameter of 5.7 mm with a 2-mm suction channel to enable adequate suction, which limits the tracheal tube to those larger than 7.5–8.0 mm, and even with an 8.0-mm tube, the bronchoscope occupies more than 50% of the tube diameter, which can lead to ventilation issues during bronchoscopy.

The authors conclude by recommending:


‘If admission to ICU is contemplated then the time-honoured ‘8.0 for females, 9.0 for males’ is a reasonable rule of thumb, unless circumstances dictate otherwise, e.g. in difficult airways or particularly small patients.’

Size matters: choosing the right tracheal tube
Anaesthesia. 2012 Aug;67(8):815-9

All Updates, ICU, PHARM, Resus, Trauma

The Bleeding Trauma Patient

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The Bleeding Trauma Patient
by Dr Pete Sherren
By popular request, Here are the slides from a presentation given by HEMS critical care physician Dr Pete Sherren.

These notes accompany the slides:
Hypothermia, acidaemia and coagulopathy or the ‘lethal triad’, is a well described entity in the trauma population and is associated with significant mortality [1]. Traditionally the aetiology of a trauma induced coagulopathy was thought to be multifactorial and involve hypothermia, acidaemia, dilutional coagulopathy, pre-existing bleeding diathesis and disseminated intravascular coagulation (Figure 1).

Figure 1. A diagram showing some of the mechanisms leading to coagulopathy in the injured.

In 2003 Brohi et al showed that around 25% of severely injured trauma patients present to hospital with a significant coagulopathy which was unrelated to fluid administration [2]. This early coagulopathy has become known as the Acute Traumatic coagulopathy (ATC) or Acute Coagulopathy of Trauma Shock (ACoTS). It is associated with an increase in transfusion requirements, injury severity scores, organ dysfunction and mortality rates [2-5].
ATC is an impairment of haemostasis involving a dynamic interaction between endogenous anticoagulants and fibrinolysis that is initiated immediately after an injury [5]. ATC is driven by an endothelial injury and hypoperfusion, which results in in increased thrombomodulin expression and activation of protein C (Figure 3). The inhibitory effect of activated protein C on clotting factors V/VIII and plasminogen activator inhibitor-1 (PAI-1), would appear key in the development of ATC [5,6].

Figure 2. Expression of thrombomodulin following a traumatic injury results in increased activation of protein C with resulting impairment of clotting factors V/VIII and reduction in thrombin generation. Activated Protein C also has an inhibitory effect on PAI-1 which results in unregulated tPA activity and fibrinolysis.

Damage control resuscitation (DCR) describes a package of care for the haemorrhaging trauma patient. It involves early damage control surgery, haemostatic resuscitation and permissive hypotension. DCR aims to control haemorrhage early while aggressively targeting the ATC and lethal triad. DCR has emerged as the accepted standard of care and some observational studies have suggested a survival benefit [6].

  • Damage Control Surgery – The priority for any haemorrhaging trauma patient is good haemostasis. Unstable patients with major trauma do not tolerate prolonged definitive surgery and hence the emergence of damage control surgery. The aim of damage control surgery is to normalise physiology at the expense of anatomy.
  • Haemostatic resuscitation – Describes the aggressive early use of packed red blood cells, clotting products and coagulation adjuncts in an attempt to mitigate the effects of the ATC and lethal triad in major trauma patients. The exact PRBC:FFP ratio remains unclear, but should ideally be less than 2:1 [7]. In massive transfusions along with appropriate FFP, platelet and fibrinogen supplementation, consideration should be given to early adjunctive therapies such as tranexamic acid [8] while maintaining ionised calcium levels greater than 1.0 mmol/L [9].
  • Permissive hypotension – Involves titrated volume resuscitation, which targets a subnormal end point that maintains organ viability until haemorrhage is controlled. By avoiding overzealous fluid resuscitation which targets normotension, the hope is to preserve the first and often best clot. Although permissive hypotension is frequently employed in traumatic haemorrhage, there is really only robust evidence that it is advantageous in penetrating trauma [10]. In blunt trauma there is a relative paucity of good evidence to guide practice, while strong evidence exists for maintaining cerebral perfusion pressures when there are associated head injuries. The end points for resuscitation will depend on age, premorbid autoregulatory state and acute pathology.

DCR is an ever evolving concept and potential emerging management strategies include –

  • Thromboelastometry (TEG/ROTEM) to guide haemostatic resuscitation instead of ratio based transfusions.
  • Prothrombin complex concentrate (FII, VII, IX and X) in non-warfarin patients
  • Fibrinogen complex concentrate (fibrinogen and FXIII) over cryoprecipitate.
  • Alkalising agents such as Tris-hydroxymethyl aminomethane (THAM) in massive transfusion with severe acidaemia
  • Novel hybrid resuscitation strategies.
  • High flow/low pressure resuscitation – endothelial resuscitation and microvascular washout.
  • Suspended Animation
  • Platelet function analysis in trauma with platelet mapping and aggregometry vs traditional PF-100

Learning points

  • Early coagulation dysfunction is common in trauma patients with haemorrhagic shock.
  • Tailored management of the ‘lethal triad’ and ATC is essential.
  • DCR is an emerging standard of care; however, some of its components are pushing the boundaries of what is good evidence based medicine.

References
1. Moore EE. Staged laparotomy for the hypothermia, acidosis, and coagulopathy. Am J Surg 1996;172:405-410.
2. Brohi K, Singh J, Heron M, Coats T. Acute Traumatic coagulopathy. J Trauma. 2003;54:1127-1130.
3. Davenport R, Manson J, De’Arth H, Platton S, Coates A, Allard S, Hart D, Pearse RM, Pasi J, MacCullum P, Stanworth S, Brohi K. Functional definition and characterization of acute traumatic coagulopathy. Crit Care Med. 2011;39(12):2652-2658.
4. Maegele M, Lefering R, Yucei N, Tjardes T, Rixen D,Paffrath T, Simanski C, Neugebauer E, Bouillon B; AG Polytrauma of the German Trauma Society (DGU). Early coagulopathy in multiple injury: an analysis from the German Trauma Registry on 8724 patients. Injury. 2007 Mar;38(3):298-304.
5. Firth D, Davenport R, Brohi K. Acute traumatic coagulopathy. Curr Opin Anaesthesiol. 2012 Apr;25(2):229-34.
6. Cotton BA, Reddy N, Hatch QM, LeFebvre E, Wade CE, Kozar RA, Gill BS, Albarado R, McNutt MK, Holcomb JB. Damage control resuscitation is associated with a reduction in resuscitation volumes and improvement in survival in 390 damage control laparotomy patients. Ann Surg. 2011 Oct;254(4):598-605.
7. Davenport R, Curry N, Manson J, De’Ath H, Coates A, Rourke C, Pearse R, Stanworth S, Brohi K. Hemostatic effects of fresh frozen plasma may be maximal at red cell ratios of 1:2. J Trauma. 2011 Jan;70(1):90-5; discussion 95-6.
8. CRASH-2 collaborators, Roberts I, Shakur H, Afolabi A, Brohi K, Coats T, Dewan Y, Gando S, Guyatt G, Hunt BJ, Morales C, Perel P, Prieto-Merino D, Woolley T. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. Lancet. 2011 Mar 26;377(9771):1096-101, 1101.e1-2.
9. Dawes R, Thomas GO. Battlefield resuscitation. Curr Opin Crit Care. 2009 Dec;15(6):527-35
10. Bickell WH, Wall MJ Jr, Pepe PE, Martin RR, Ginger VF, Allen MK, Mattox KL. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994 Oct 27;331(17):1105-9.
11. Schöchl H, Maegele M, Solomon C, Görlinger K, Voelckel W. Early and individualized goal-directed therapy for trauma-induced coagulopathy. Scand J Trauma Resusc Emerg Med. 2012 Feb 24;20:15.

Acute Med, All Updates, ICU

Unknown unknowns and pleural effusions

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There are plenty of unknowns when it comes to management of pleural effusions on the ICU, which led to a paper with an eye-catching title1.
Mechanically ventilated patients frequently have pleural effusions detected by radiological investigations. Whether to drain them is a common conundrum for intensivists. A systematic review of the literature showed that drainage often improves oxygenation and has a low complication rate2.
While it may have the added advantage of assisting diagnosis and guiding therapy, there is a paucity of literature demonstrating improved patient-orientated outcomes with the routine drainage of pleural effusions in ventilated patients.
 
1. A pseudo-Rumsfeldian approach to pleural effusions in mechanically ventilated patients.
Crit Care. 2011 Mar 11;15(2):132 Free Full Text
2. Utility and safety of draining pleural effusions in mechanically ventilated patients: a systematic review and meta-analysis.
Crit Care. 2011;15(1):R46 Free Full Text
[EXPAND Click to read abstract]

INTRODUCTION: Pleural effusions are frequently drained in mechanically ventilated patients but the benefits and risks of this procedure are not well established.

METHODS: We performed a literature search of multiple databases (MEDLINE, EMBASE, HEALTHSTAR, CINAHL) up to April 2010 to identify studies reporting clinical or physiological outcomes of mechanically ventilated critically ill patients who underwent drainage of pleural effusions. Studies were adjudicated for inclusion independently and in duplicate. Data on duration of ventilation and other clinical outcomes, oxygenation and lung mechanics, and adverse events were abstracted in duplicate independently.

RESULTS: Nineteen observational studies (N = 1,124) met selection criteria. The mean PaO2:FiO2 ratio improved by 18% (95% confidence interval (CI) 5% to 33%, I2 = 53.7%, five studies including 118 patients) after effusion drainage. Reported complication rates were low for pneumothorax (20 events in 14 studies including 965 patients; pooled mean 3.4%, 95% CI 1.7 to 6.5%, I2 = 52.5%) and hemothorax (4 events in 10 studies including 721 patients; pooled mean 1.6%, 95% CI 0.8 to 3.3%, I2 = 0%). The use of ultrasound guidance (either real-time or for site marking) was not associated with a statistically significant reduction in the risk of pneumothorax (OR = 0.32; 95% CI 0.08 to 1.19). Studies did not report duration of ventilation, length of stay in the intensive care unit or hospital, or mortality.

CONCLUSIONS: Drainage of pleural effusions in mechanically ventilated patients appears to improve oxygenation and is safe. We found no data to either support or refute claims of beneficial effects on clinically important outcomes such as duration of ventilation or length of stay.

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