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…
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.
‘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.’
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.”
“…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.
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.
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)?
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.
For patients who will be having a chest CT, perhaps sonography could replace chest radiography in the resus room as the initial imaging step; this recent prospective study shows its superiority over the ‘traditional’ ATLS approach.
In haemodynamically stable patients with prophylactic pelvic splints in place, one could easily argue against plain pelvis films too (the caveat being rapid access to CT is necessary). The arguments against resus-room lateral cervical spine x-rays were made ages ago and these are now rarely done in the UK & Australia.
Is it time to abandon plain radiography altogether for stable major trauma patients?
Background: The accuracy of combined clinical examination (CE) and chest radiography (CXR) (CE + CXR) vs thoracic ultrasonography in the acute assessment of pneumothorax, hemothorax, and lung contusion in chest trauma patients is unknown.
Methods: We conducted a prospective, observational cohort study involving 119 adult patients admitted to the ED with thoracic trauma. Each patient, secured onto a vacuum mattress, underwent a subsequent thoracic CT scan after first receiving CE, CXR, and thoracic ultrasonography. The diagnostic performance of each method was also evaluated in a subgroup of 35 patients with hemodynamic and/or respiratory instability.
Results: Of the 237 lung fields included in the study, we observed 53 pneumothoraces, 35 hemothoraces, and 147 lung contusions, according to either thoracic CT scan or thoracic decompression if placed before the CT scan. The diagnostic performance of ultrasonography was higher than that of CE + CXR, as shown by their respective areas under the receiver operating characteristic curves (AUC-ROC): mean 0.75 (95% CI, 0.67-0.83) vs 0.62 (0.54-0.70) in pneumothorax cases and 0.73 (0.67-0.80) vs 0.66 (0.61-0.72) for lung contusions, respectively (all P < .05). In addition, the diagnostic performance of ultrasonography to detect pneumothorax was enhanced in the most severely injured patients: 0.86 (0.73-0.98) vs 0.70 (0.61-0.80) with CE + CXR. No difference between modalities was found for hemothorax.
Conclusions: Thoracic ultrasonography as a bedside diagnostic modality is a better diagnostic test than CE and CXR in comparison with CT scanning when evaluating supine chest trauma patients in the emergency setting, particularly for diagnosing pneumothoraces and lung contusions.
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.’