Tag Archives: critical care

All Updates, ICU, Resus

Delta CVP with PEEP and fluid responsiveness

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I’ve been (and remain) critical of the use of CVP to determine ‘filling status’ or more accurately volume-responsiveness, even using CVP trends; I’m generally in agreement with Dr Marik’s bold statement that “CVP should not be used to make clinical decisions regarding fluid management”1. However there might now appear to be a way of using CVP for this purpose.
Increasing PEEP in patients undergoing positive pressure ventilation can increase the CVP. It has been demonstrated in a small study of cardiac surgical patients2 that the degree to which a 10cmH2O increase in PEEP changes the CVP correlates with fluid responsiveness. The fluid responsiveness was determined by the change in cardiac output measured by thermodilution after a passive leg raise.
There are a number of limitations to this study that should prevent us from immediately extrapolating this method of determining fluid responsiveness to our ED / critical care patients, but the concept is interesting. This can be added to the growing pile of dynamic measures of circulatory filling.


Background Changes in central venous pressure (CVP) rather than absolute values may be used to guide fluid therapy in critically ill patients undergoing mechanical ventilation. We conducted a study comparing the changes in the CVP produced by an increase in PEEP and stroke volume variation (SVV) as indicators of fluid responsiveness. Fluid responsiveness was assessed by the changes in cardiac output (CO) produced by passive leg raising (PLR).

Methods In 20 fully mechanically ventilated patients after cardiac surgery, PEEP was increased +10 cm H2O for 5 min followed by PLR. CVP, SVV, and thermodilution CO were measured before, during, and directly after the PEEP challenge and 30° PLR. The CO increase >7% upon PLR was used to define responders.

Results Twenty patients were included; of whom, 10 responded to PLR. The increase in CO by PLR directly related (r=0.77, P<0.001) to the increase in CVP by PEEP. PLR responsiveness was predicted by the PEEP-induced increase in CVP [area under receiver-operating characteristic (AUROC) curve 0.99, P<0.001] and by baseline SVV (AUROC 0.90, P=0.003). The AUROC's for dCVP and SVV did not differ significantly (P=0.299).
Conclusions Our data in mechanically ventilated, cardiac surgery patients suggest that the newly defined parameter, PEEP-induced CVP changes, like SVV, appears to be a good parameter to predict fluid responsiveness.

1. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares.
Chest. 2008 Jul;134(1):172-8
Full Text Link
2. Predicting cardiac output responses to passive leg raising by a PEEP-induced increase in central venous pressure, in cardiac surgery patients.
Br J Anaesth. 2011 Aug;107(2):251-7

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

Capillary refill time

A review of capillary refill time (CRT) reveals some interesting details about this test:

  • CRT is affected by age – the upper limit of normal for neonates is 3 seconds.
  • It increases with age – one study recommended the upper limit of normal for adult women should be increased to 2.9 seconds and for the elderly to 4.5 seconds.
  • It is affected by multiple external factors (especially ambient temperature).
  • Although it is claimed to have some predictive value in the assessment of dehydration and serious infection in children, studies vary in where and for how long pressure should be applied, and there is poor interobserver reliability.

The latest (5th Edition) of the Advanced Paediatric Life Support Manual states:
‘Poor capillary refill and differential pulse volumes are neither sensitive nor specific indicators of shock in infants and children, but are useful clinical signs when used in conjunction with the other signs described‘
In my view, it is best used as a monitor of trends (in accordance with skin temperature and other markers of perfusion), rather than by placing emphasis on the exact number of seconds of a single reading. See below for a video of my perfectly happy and healthy son demonstrating a CRT of over six seconds in a cool room during an English Summer’s day.
The authors of the review caution:
Operating rooms are cold, patients are often draped, which limits access, and because most anesthetics are potent vasodilators, the use of CRT to guide practice is not justified. The possibility of a false-positive or false-negative assessment is simply too great.


Capillary refill time (CRT) is widely used by health care workers as part of the rapid, structured cardiopulmonary assessment of critically ill patients. Measurement involves the visual inspection of blood returning to distal capillaries after they have been emptied by pressure. It is hypothesized that CRT is a simple measure of alterations in peripheral perfusion. Evidence for the use of CRT in anesthesia is lacking and further research is required, but understanding may be gained from evidence in other fields. In this report, we examine this evidence and factors affecting CRT measurement. Novel approaches to the assessment of CRT are under investigation. In the future, CRT measurement may be achieved using new technologies such as digital videography or modified oxygen saturation probes; these new methods would remove the limitations associated with clinical CRT measurement and may even be able to provide an automated CRT measurement.

Capillary Refill Time: Is It Still a Useful Clinical Sign?
Anesth Analg. 2011 Jul;113(1):120-3
The Capillary Refill Video

Acute Med, All Updates, ICU, Kids, Resus

Why I don't give vasopressors in sepsis

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It’s become popular to use the term ‘vasopressors’ or just ‘pressors’ when noradrenaline/norepinephrine or even (in some places still) dopamine are given. I have resisted this trend and continue to use the term ‘vasoactive’ drugs, on the basis that the effects they produce (and that we may desire) are not limited to a pure alpha adrenergic effect on vascular tone, but they have effects on heart rate and contractility too (as well as preload through venous effects). If you don’t believe me about noradrenaline/norepinephrine, then check out one of my favourite critical care papers of all time: the CAT study.
There are of course real pressors out there – phenylephrine acts on alpha receptors, as does methoxamine. Metaraminol predominantly acts on alpha receptors but does also cause some release of noradrenaline/norepinephrine.
Why is this important? All these drugs will fix hypotension, right? Yes, they should. However should blood pressure be our main treatment goal? What we’re really interested in is organ perfusion, which depends on regional blood flow to vital organs. It’s possible that a drug could fix the measured blood pressure and give a nice ‘macroscopic’ number, while at the same time reducing cardiac output and adversely affecting regional blood flow to organs through local vasoconstrictive effects. My view is that this is more likely with pure ‘pressors’ (like phenylephrine), which is why I avoid them in septic shock and opt for catecholamine infusions (noradrenaline/norepinephrine).
This is important in my practice setting of retrieval medicine, where, prior to interfacility transport, physicians might sometimes be tempted to ‘push pressors’ peripherally rather than insert a central venous catheter and commence a catecholamine infusion. While the former approach might be more expeditious and make the vital signs chart look pretty, one wonders about what effect this is having on tissue oxygen delivery.
A fascinating review of papers on pressor physiology1 suggests these agents have the following effects:

  • conflicting data on changes in myocardial perfusion
  • increase both left and right heart afterload
  • decrease venous compliance with the potential to increase venous return although the impact of this on cardiac output is controversial
  • controversial effect on cerebral bloodflow
  • decrease bloodflow to the kidneys
  • adverse affects on gastrointestinal tract bloodflow


abstract1
Phenylephrine and methoxamine are direct-acting, predominantly α(1) adrenergic receptor (AR) agonists. To better understand their physiologic effects, we screened 463 articles on the basis of PubMed searches of “methoxamine” and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Both methoxamine and phenylephrine increase cardiac afterload via several mechanisms, including increased vascular resistance, decreased vascular compliance, and disadvantageous alterations in the pressure waveforms produced by the pulsatile heart. Although pure α(1) agonists increase arterial blood pressure, neither animal nor human studies have ever shown pure α(1)-agonism to produce a favorable change in myocardial energetics because of the resultant increase in myocardial workload. Furthermore, the cost of increased blood pressure after pure α(1)-agonism is almost invariably decreased cardiac output, likely due to increases in venous resistance. The venous system contains α(1) ARs, and though stimulation of α(1) ARs decreases capacitance and may transiently increase venous return, this gain may be offset by changes in afterload, venous compliance, and venous resistance. Data on the effects of α(1) stimulation in the central nervous system show conflicting changes, while experimental animal data suggest that renal blood flow is reduced by α(1)-agonists, and both animal and human data suggest that gastrointestinal perfusion may be reduced by α(1) tone.

A review of clinical articles2 reveals few evidence-based indications for true pressors. Possible situations where they may be of benefit include intraoperative hypotension, aortic stenosis, during cyanotic episodes in Tetralogy of Fallot, and some obstetric situations. In the setting of sepis, phenylephrine has been compared with noradrenaline in which an initial pilot study found a statistically significant reduction in creatinine clearance and increase in arterial lactate after initiating the phenylephrine infusion. However a subsequent randomised controlled comparison of phenylephrine with noradrenaline/norepinephrine did not show differences in cardiopulmonary performance, global oxygen transport, or regional hemodynamics, although there were only 16 patients in each group3.


abstract2
Phenylephrine is a direct-acting, predominantly α(1) adrenergic receptor agonist used by anesthesiologists and intensivists to treat hypotension. A variety of physiologic studies suggest that α-agonists increase cardiac afterload, reduce venous compliance, and reduce renal bloodflow. The effects on gastrointestinal and cerebral perfusion are controversial. To better understand the effects of phenylephrine in a variety of clinical settings, we screened 463 articles on the basis of PubMed searches of “methoxamine,” a long-acting α agonist, and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Phenylephrine has been studied as an antihypotensive drug in patients with severe aortic stenosis, as a treatment for decompensated tetralogy of Fallot and hypoxemia during 1-lung ventilation, as well as for the treatment of septic shock, traumatic brain injury, vasospasm status-postsubarachnoid hemorrhage, and hypotension during cesarean delivery. In specific instances (critical aortic stenosis, tetralogy of Fallot, hypotension during cesarean delivery) in which the regional effects of phenylephrine (e.g., decreased heart rate, favorable alterations in Q(p):Q(s) ratio, improved fetal oxygen supply:demand ratio) outweigh its global effects (e.g., decreased cardiac output), phenylephrine may be a rational pharmacologic choice. In pathophysiologic states in which no regional advantages are gained by using an α(1) agonist, alternative vasopressors should be sought.

These review articles reinforce my own bias against the use of pure pressors in septic shock, although clearly more clinical research is needed. I am inclined to agree with the reviewers’ concluding statement:
…in all clinical settings, phenylephrine reduces cardiac output, and in most clinical settings has been shown to significantly increase LV afterload. Thus, only in instances in which its regional effects are thought to outweigh its global effects should phenylephrine be used for the treatment of hypotension.
1. The physiologic implications of isolated alpha(1) adrenergic stimulation
Anesth Analg. 2011 Aug;113(2):284-96
2. The clinical implications of isolated alpha(1) adrenergic stimulation
Anesth Analg. 2011 Aug;113(2):297-304
3. Phenylephrine versus norepinephrine for initial hemodynamic support of patients with septic shock: a randomized, controlled trial
Crit Care. 2008;12(6):R143
Full Text available here

Acute Med, All Updates, PHARM, Resus

Pre-hospital CPAP for pulmonary oedema

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The physician-staffed mobile intensive care units of SAMU (Service d’Aide Médicale Urgente) in France provided the location for this randomised controlled trial of CPAP for acute cardiogenic pulmonary oedema.


STUDY OBJECTIVE: The purpose of this randomized controlled trial was to determine the immediate and delayed effects of noninvasive ventilation for patients in acute cardiogenic pulmonary edema (ACPE) in addition to aggressive usual care in a medical prehospital setting.

METHODS: Out-of-hospital patients in severe ACPE were eligible for the study. Patients were randomized to receive either usual care, including conventional optimal treatment with furosemide, oxygen, and high-dose boluses of isosorbide dinitrate plus oxygen, or conventional medications plus out-of-hospital continuous positive airway pressure (CPAP). The primary outcome was the treatment success defined as all of respiratory rate less than 25 breaths per minute and oxygen saturation of greater than 90% at the end of 1-hour study. Secondary end points included death during 30 days after inclusion. Lengths of intensive care unit and hospital stays were also recorded.

RESULTS: In total, 124 patients were enrolled into the study. The 2 groups had similar baseline characteristics. For the primary outcome analysis, 22 (35.5%) of 62 patients were considered as experiencing a treatment success in the usual care group vs 19 (31.7%) of 60 in the CPAP group (P = .65). Seven patients died within 30 days in the usual care group vs 6 in the CPAP group (P = .52). There were no statistically significant differences between the treatment groups for length of stay either in hospital or in the intensive care unit.

CONCLUSION: In the prehospital setting, in spite of its potential advantages for patients in ACPE, CPAP may not be preferred to a strict optimal intravenous treatment.

Continuous positive airway pressure for cardiogenic pulmonary edema: a randomized study
Am J Emerg Med. 2011 Sep;29(7):775-81

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

Still no cardiac arrest survival benefit from epinephrine?

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A double blind randomised controlled trial showed significantly better rates of return of spontaneous circulation and hospital admission with the use of adrenaline (epinephrine) compared with placebo. This effect was observed with both shockable and non-shockable initial cardiac arrest rhythms. There was no statistically significant difference in the primary outcome of survival to hospital discharge.
Interesting but unfortunate political factors appear to have prevented recruitment to the required numbers of patients for this study so it is underpowered for its primary outcome of survival to hospital discharge, which in the adrenaline group was double that in the placebo group, although this did not reach statistical significance. What was supposed to be a multi-centre study became a single centre one and it was not possible to continue as the study drugs reached their expiry date and no additional funding was available.
So do ROSC and survival to admission matter? The authors make the following point:


While not the primary outcome of our study, ROSC is an increasingly important clinical endpoint as the influence of post resuscitation care interventions (i.e.: therapeutic hypothermia, managing underlying cause, organ perfusion and oxygenation) on survival to hospital discharge are recognised.

Optimum dose and timing of adrenaline remain unknown, along with whether it impacts on long-term outcomes.


BACKGROUND: There is little evidence from clinical trials that the use of adrenaline (epinephrine) in treating cardiac arrest improves survival, despite adrenaline being considered standard of care for many decades. The aim of our study was to determine the effect of adrenaline on patient survival to hospital discharge in out of hospital cardiac arrest.

METHODS: We conducted a double blind randomised placebo-controlled trial of adrenaline in out-of-hospital cardiac arrest. Identical study vials containing either adrenaline 1:1000 or placebo (sodium chloride 0.9%) were prepared. Patients were randomly allocated to receive 1ml aliquots of the trial drug according to current advanced life support guidelines. Outcomes assessed included survival to hospital discharge (primary outcome), pre-hospital return of spontaneous circulation (ROSC) and neurological outcome (Cerebral Performance Category Score – CPC).

RESULTS: A total of 4103 cardiac arrests were screened during the study period of which 601 underwent randomisation. Documentation was available for a total of 534 patients: 262 in the placebo group and 272 in the adrenaline group. Groups were well matched for baseline characteristics including age, gender and receiving bystander CPR. ROSC occurred in 22 (8.4%) of patients receiving placebo and 64 (23.5%) who received adrenaline (OR=3.4; 95% CI 2.0-5.6). Survival to hospital discharge occurred in 5 (1.9%) and 11 (4.0%) patients receiving placebo or adrenaline respectively (OR=2.2; 95% CI 0.7-6.3). All but two patients (both in the adrenaline group) had a CPC score of 1-2.

CONCLUSION: Patients receiving adrenaline during cardiac arrest had no statistically significant improvement in the primary outcome of survival to hospital discharge although there was a significantly improved likelihood of achieving ROSC.

Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Resuscitation. 2011 Sep;82(9):1138-43

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

Pre-hospital ECMO

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Two cases are reported of the pre-hospital institution of venoarterial extracorporeal membrane oxygenation (ECMO) for patients in cardiac arrest. One was from France and the other from Germany – both countries with mature physician-staffed pre-hospital systems. The two cases were a 9 yr old drowning victim1 and a 48 year old marathon runner2. They each received BLS then ACLS then ECMO, and both went from asystole to sinus rhythm after the institution of ECMO. Sadly both failed to neurologically recover and died in hospital.
If irreversible anoxic encephalopathy could be detected in the field, patients could be better selected for this intervention. An editorialist3 states:


Until we have a hand held device which can measure neuronal integrity on a cellular level in the field we must use our best judgement, and in many cases give the patient the benefit of the doubt by cannulating them, cooling for 24 h and then making a neurological assessment and withdrawing ECLS if necessary.

Other issues to consider are:

  • Can society afford this level of intervention?
  • Could this intervention, when associated with brain death, result in sufficiently recovered organs for transplantation?
  • How can the infrastructure be created to enable rapid institution of pre-hospital ECMO?

I suspect as the equipment becomes even more portable and self-maintaining, pre-hospital / retrieval physicians already expert in critical care interventions such as seldinger-guided vascular access will be the ones instituting this therapy. In the meantime, we await evidence of outcome benefit and some objective means of case selection.
1. Out-of-hospital extracorporeal life support for cardiac arrest—A case report
Resuscitation. 2011 Sep;82(9):1243-5
2. Out-of-hospital extra-corporeal life support implantation during refractory cardiac arrest in a half-marathon runner
Resuscitation. 2011 Sep;82(9):1239-42
3. Community extracorporeal life support for cardiac arrest – When should it be used?
Resuscitation. 2011 Sep;82(9):1117

Acute Med, All Updates, PHARM, Resus

Mouth-to-nose breathing

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Interesting – mouth to nose breathing was more effective than mouth-to-mouth in simulated resuscitations using anaesthetised, apnoeic patients:


BACKGROUND: The authors hypothesized that mouth ventilation by a resuscitator via the nasal route ensures a more patent airway and more effective ventilation than does ventilation via the oral route and therefore would be the optimal manner to ventilate adult patients in emergencies, such as during cardiopulmonary resuscitation. They tested the hypothesis by comparing the effectiveness of mouth-to-nose breathing (MNB) and mouth-to-mouth breathing (MMB) in anesthetized, apneic, adult subjects without muscle paralysis.

METHODS: Twenty subjects under general anesthesia randomly received MMB and MNB with their heads placed first in a neutral position and then an extended position. A single operator performed MNB and MMB at the target breathing rate of 10 breaths/min, inspiratory:expiratory ratio 1:2 and peak inspiratory airway pressure 24 cm H₂O. A plethysmograph was used to measure the amplitude change during MMB and MNB. The inspiratory and expiratory tidal volumes during MMB and MNB were calculated retrospectively using the calibration curve.

RESULTS: All data are presented as medians (interquartile ranges). The rates of effective ventilation (expired volume > estimated anatomic dead space) during MNB and MMB were 91.1% (42.4-100%) and 43.1% (42.5-100%) (P < 0.001), and expired tidal volume with MMB 130.5 ml (44.0-372.8 ml) was significantly lower than with MNB 324.5 ml (140.8-509.0 ml), regardless of the head position (P < 0.001).
CONCLUSIONS: Direct mouth ventilation delivered exclusively via the nose is significantly more effective than that delivered via the mouth in anesthetized, apneic adult subjects without muscle paralysis. Additional studies are needed to establish whether using this breathing technique during emergency situations will improve patient outcomes.

Effectiveness of breathing through nasal and oral routes in unconscious apneic adult human subjects: a prospective randomized crossover trial
Anesthesiology. 2011 Jul;115(1):129-35

All Updates, ICU

Glutamine in ICU

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Of interest to intensivists….


Background: Low plasma glutamine concentration is an independent prognostic factor for an unfavourable outcome in the intensive care unit (ICU). Intravenous (i.v.) supplementation with glutamine is reported to improve outcome. In a multi-centric, double-blinded, controlled, randomised, pragmatic clinical trial of i.v. glutamine supplementation for ICU patients, we investigated outcomes regarding sequential organ failure assessment (SOFA) scores and mortality. The hypothesis was that the change in the SOFA score would be improved by glutamine supplementation.

Methods: Patients (n=413) given nutrition by an enteral and/or a parenteral route with the aim of providing full nutrition were included within 72 h after ICU admission. Glutamine was supplemented as i.v. l-alanyl-l-glutamine, 0.283 g glutamine/kg body weight/24 h for the entire ICU stay. Placebo was saline in identical bottles. All included patients were considered as intention-to-treat patients. Patients given supplementation for >3 days were considered as predetermined per protocol (PP) patients.

Results: There was a lower ICU mortality in the treatment arm as compared with the controls in the PP group, but not at 6 months. For change in the SOFA scores, no differences were seen, 1 (0,3) vs. 2 (0.4), P=0.792, for the glutamine group and the controls, respectively.

Conclusion: In summary, a reduced ICU mortality was observed during i.v. glutamine supplementation in the PP group. The pragmatic design of the study makes the results representative for a broad range of ICU patients.

Scandinavian glutamine trial: a pragmatic multi-centre randomised clinical trial of intensive care unit patients
Acta Anaesthesiol Scand. 2011 Aug;55(7):812-818

Acute Med, All Updates, ICU, Resus

Nitric oxide for right ventricular cardiogenic shock

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A case report describes a patient with right ventricular cardiogenic shock due to a dissected right coronary artery1. There was deterioration despite fluid, inotropic and intraaortic balloon pump therapy, followed by improvement with the introduction of inhaled nitric oxide (iNO) at 12 to 15 ppm (a selective pulmonary vasodilator), to the point where vasoactive medication was withdrawn. The cessation of iNO was associated with deterioration which resolved with its reintroduction. It was more gradually withdrawn and the patient made a good recovery.
The rationale for the use of iNO in patients with acute RV heart failure due to MI is afterload reduction without systemic hypotension.
It has been shown to improve haemodynamics in RV MI patients with cardiogenic shock in a previous case series2 (abstract below) in which its effects on pulmonary vasodilation are thought be beneficial. In RV MI with shock increased pulmonary vascular tone is postulated to result from the following mechanisms:

  • A low cardiac output results in a decreased mixed venous blood oxygen content, which enhances pulmonary artery vasoconstriction.
  • The intravenous infusion of alpha-adrenergic vasoconstrictors can contribute to pulmonary vasoconstriction.
  • Mechanical ventilation with positive end-expiratory pressure can increase the pulmonary vascular resistance through compression of the pulmonary vasculature.
  • Interstitial pulmonary edema, which may occur in some patients with coexisting LV dysfunction, can also cause pulmonary constriction

OBJECTIVES: We sought to determine whether or not inhaled nitric oxide (NO) could improve hemodynamic function in patients with right ventricular myocardial infarction (RVMI) and cardiogenic shock (CS).

BACKGROUND: Inhaled NO is a selective pulmonary vasodilator that can decrease right ventricular afterload.

METHODS: Thirteen patients (7 males and 6 females, age 65 +/- 3 years) presenting with electrocardiographic, echocardiographic, and hemodynamic evidence of acute inferior myocardial infarction associated with RVMI and CS were studied. After administration of supplemental oxygen (inspired oxygen fraction [F(i)O(2)] = 1.0), hemodynamic measurements were recorded before, during inhalation of NO (80 ppm at F(i)O(2) = 0.90) for 10 min, and 10 min after NO inhalation was discontinued (F(i)O(2) = 1.0).

RESULTS: Breathing NO decreased the mean right atrial pressure by 12 +/- 3%, mean pulmonary arterial pressure by 13 +/- 2%, and pulmonary vascular resistance by 36 +/- 8% (all p < 0.05). Nitric oxide inhalation increased the cardiac index by 24 +/- 11% and the stroke volume index by 23 +/- 12% (p < 0.05). The NO administration did not change systemic arterial or pulmonary capillary wedge pressures. Contrast echocardiography identified three patients with a patent foramen ovale and right-to-left shunt flow while breathing at F(i)O(2) = 1.0. Breathing NO decreased shunt flow by 56 +/- 5% (p < 0.05) and was associated with markedly improved systemic oxygen saturation.

CONCLUSIONS: Nitric oxide inhalation results in acute hemodynamic improvement when administered to patients with RVMI and CS.

1. Use of inhaled nitric oxide in the treatment of right ventricular myocardial infarction
Am J Emerg Med. 2011 May;29(4):473.e3-5
2. Hemodynamic effects of inhaled nitric oxide in right ventricular myocardial infarction and cardiogenic shock
J Am Coll Cardiol. 2004 Aug 18;44(4):793-8

All Updates, ICU, Resus, Ultrasound

Ultrasound to detect difficult laryngoscopy

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A pilot study suggests sonographic measurements of neck soft tissue thickness may predict difficult laryngoscopy. Laryngoscopy was difficult in patients with increased thickness of the anterior neck soft tissue at the level of the hyoid bone and thyrohyoid membrane. The authors suggest that anterior neck soft tissue thickness cutoff value of 2.8 cm at the thyrohyoid membrane level can potentially be used to detect difficult laryngoscopy, but that this would require further validation since in this pilot study there were only six subjects in the difficult laryngoscopy group.


Objectives:  Prediction of difficult laryngoscopy in emergency care settings is challenging. The preintubation clinical screening tests may not be applied in a large number of emergency intubations due to the patient’s clinical condition. The objectives of this study were 1) to determine the utility of sonographic measurements of thickness of the tongue, anterior neck soft tissue at the level of the hyoid bone, and thyrohyoid membrane in distinguishing difficult and easy laryngoscopies and 2) to examine the association between sonographic measurements (thickness of tongue and anterior neck soft tissue) and difficult airway clinical screening tests (modified Mallampati score, thyromental distance, and interincisor gap).

Methods:  This was a prospective observational study at an academic medical center. Adult patients undergoing endotracheal intubation for an elective surgical procedure were included. The investigators involved in data collection were blinded to each other’s assessments. Demographic variables were collected preoperatively. The clinical screening tests to predict a difficult airway were performed. The ultrasound (US) measurements of tongue and anterior neck soft tissue were obtained. The laryngoscopic view was graded using Cormack and Lehane classification by anesthesia providers on the day of surgery. To allow for comparisons between difficult airway and easy airway groups, a two-sided Student’s t-test and Fisher’s exact test were employed as appropriate. Spearman’s rank correlation coefficients were used to examine the association between screening tests and sonographic measurements.

Results:  The mean (±standard deviation [SD]) age of 51 eligible patients (32 female, 19 male) was 53.1 (±13.2) years. Six of the 51 patients (12%, 95% confidence interval [CI] = 3% to 20%) were classified as having difficult laryngoscopy by anesthesia providers. The distribution of laryngoscopy grades for all subjects was 63, 25, 4, and 8% for grades 1, 2, 3, and 4, respectively. In this study, 83% of subjects with difficult airways were males. No other significant differences were noted in the demographic variables and difficult airway clinical screening tests between the two groups. The sonographic measurements of anterior neck soft tissue were greater in the difficult laryngoscopy group compared to the easy laryngoscopy group at the level of the hyoid bone (1.69, 95% CI = 1.19 to 2.19 vs. 1.37, 95% CI = 1.27 to 1.46) and thyrohyoid membrane (3.47, 95% CI = 2.88 to 4.07 vs. 2.37, 95% CI = 2.29 to 2.44). No significant correlation was found between sonographic measurements and clinical screening tests.

Conclusions:  This pilot study demonstrated that sonographic measurements of anterior neck soft tissue thickness at the level of hyoid bone and thyrohyoid membrane can be used to distinguish difficult and easy laryngoscopies. Clinical screening tests did not correlate with US measurements, and US was able to detect difficult laryngoscopy, indicating the limitations of the conventional screening tests for predicting difficult laryngoscopy.

Pilot Study to Determine the Utility of Point-of-care Ultrasound in the Assessment of Difficult Laryngoscopy
Acad Emerg Med. 2011 Jul;18(7):754-8