Tag Archives: critical care

Hypothermia and hypokalaemia

We all like to treat selected post cardiac arrest patients with hypothermia now, but isn’t hypothermia associated with a drop in potassium, which of course can precipitate pesky ventricular dysrhythmias in patients who would really rather not arrest again. Maybe the hypothermia itself is protective against the dysrhythmias?
A study from the Mayo Clinic updates our knowledge of this area:

METHODS: We retrospectively analyzed potassium variability with Therapeutic Hypothermia (TH) and performed correlative analysis of QT intervals and the incidence of ventricular arrhythmia.
RESULTS: We enrolled 94 sequential patients with OHCA, and serum potassium was followed intensively. The average initial potassium value was 3.9±0.7 mmol/l and decreased to a nadir of 3.2±0.7 mmol/l at 10 h after initiation of cooling (p<0.001). Eleven patients developed sustained polymorphic ventricular tachycardia (PVT) with eight of these occurring during the cooling phase. The corrected QT interval prolonged in relation to the development of hypothermia (p<0.001). Hypokalemia was significantly associated with the development of PVT (p=0.002), with this arrhythmia being most likely to develop in patients with serum potassium values of less than 2.5 mmol/l (p=0.002). Rebound hyperkalemia did not reach concerning levels (maximum 4.26±0.8 mmol/l at 40 h) and was not associated with the occurrence of ventricular arrhythmia. Furthermore, repletion of serum potassium did not correlate with the development of ventricular arrhythmia.
CONCLUSIONS: Therapeutic hypothermia is associated with a significant decline in serum potassium during cooling. Hypothermic core temperatures do not appear to protect against ventricular arrhythmia in the context of severe hypokalemia and cautious supplementation to maintain potassium at 3.0 mmol/l appears to be both safe and effective.
Hypokalemia during the cooling phase of therapeutic hypothermia and its impact on arrhythmogenesis
Resuscitation. 2010 Dec;81(12):1632-6

Bleeding Tracheostomy

Adapted from the UK Intensive Care Society’s ‘Standards for the care of adult patients with a temporary tracheostomy

Bleeding from an established tracheostomy (ie. ‘late bleeding’, as to opposed to peri-operative bleeding that is more common and often benign) may occur because of erosion of blood vessels in and around the stoma site. This is more likely if there has been infection of the stoma site. Such bleeding may settle with conservative management. More worryingly, however, is the prospect of such bleeding being the result of erosion of a major artery in the root of the neck where there has been pressure from the tracheostomy tube itself or the cuff tube. Most commonly, this erosion occurs into the right brachiocephalic artery (also known as the innominate artery), resulting in a tracheo-innominate artery fistula. This situation may be heralded in the preceding hours by a small, apparently insignificant, sentinel bleed. Bleeding from such a fistula will be massive. THIS IS A LIFE-THREATENING EMERGENCY and so decisions need to be rapidly made.

  1. Call for help– senior medical and nursing staff, other health professionals with tracheostomy care skills (e.g. respiratory therapist, physiotherapist).
  2. Clear airway – blood clots may need to be suctioned.
  3. Replace blood products as required
  4. Bleeding may be temporarily reduced or stopped by applying finger pressure to the root of the neck in the sternal notch, or by inflating the tracheostomy tube cuff (if present) with a 50ml syringe of air. This inflation should be done slowly and steadily to inflate the balloon to a maximum volume without bursting it. Depending on the type and size of the tracheostomy tube this may be anywhere between 10 and 35 ml.
  5. Urgent referral for surgical exploration must now be made, if not already done so. In addition to an ENT or maxillofacial surgeon, it may be necessary to get help from a vascular surgeon. Sometimes, the damage can only be repaired utilising cardio-pulmonary bypass, and so a cardiothoracic surgeon may also be needed to help.
  6. Consider palliation – it is well recognised that fatalities occur in this situation, and that this may be the mode of death for some patients with head and neck cancers

Tracheostomy resources

The National Tracheostomy Safety Project at www.tracheostomy.org.uk in the UK aims to allow patients with tracheostomies or laryngectomies to be safely cared for in hospitals.
The site contains a wealth of educational resources of use to the critical care practitioner. For example, have you thought about what do with a laryngectomy patient who presents with dyspnoea, or even apnoea? Remember that although applying oxygen to the face & neck is a default emergency action for all patients with a tracheostomy, these patients cannot be intubated and ventilated through the normal oral route since their tracheostomy is an end stoma – it does not communicate with the mouth:

Compare this with the algorithm for other patients with a tracheostomy, in whom attempts to oxygenate and ventilate, including intubation, can be made in an emergency either from the ‘top end’ (mouth) or via the stoma:

There are also a number of multimedia resources and a link to the UK Intensive Care Society’s Tracheostomy Guidelines

Percutaneous Dilatational Tracheostomy

In ICU, Percutaneous Dilatational Tracheostomy (PDT) is often performed to facilitate weaning from mechanical ventilation, reduce anatomical dead space, avoid laryngeal injury and aid in management of tracheobronchial and pulmonary secretions.
There is still controversy over optimal timing and case selection for PDT. Some organisations have helped to clarify the situation for practicing intensivists.
In 2010 the Australian and New Zealand Intensive Care Society (ANZICS) produced its Percutaneous Dilatational Tracheostomy Consensus Statement, to represent best current practice in Australia and New Zealand.
This can be downloaded from here.

Cuff pressures and tracheal injury

We all intubate patients with cuffed tubes, but we’re far too busy and important to fart around measuring tracheal tube cuff pressures when we’re saving lives right? Surely something the ICU nurses can sort out between ‘eye care’ and swabbing for MRSA.
The modern ‘high volume low pressure’ cuff has certainly led us to worry less about cuff pressures, and in frontline critical care specialties like emergency medicine and pre-hospital and retrieval medicine it’s the last thing on our minds. However we should consider the accumulating pool of evidence that tells us:

  1. Physicians are hopelessly poor at estimating cuff pressures based on palpating the pilot balloon
  2. Cuff pressures are frequently very high
  3. Tracheal mucosal injury can occur even after short term intubation (a few hours)
  4. When the pressure in the cuff exceeds 22 mm Hg, blood flow in the tracheal mucosa begins decreasing
  5. Tracheal mucosal blood flow reduces markedly when the pressure reaches 30 mm Hg
  6. When the pressure in the cuff reaches 50 mm Hg for 15 minutes, ischemic injury to the tracheal mucosa can occur

Patchy hemorrhagic ulceration in tracheal mucosa

A study from China tested the hypothesis that an appropriate tracheal tube cuff (ETTc) pressure even in short procedures would reduce endotracheal intubation–related morbidity. They compared bronchoscopic appearance of tracheal mucosa, and patient symptoms of tracheal injury, in two groups of elective surgical patients anaesthetised and intubated between 120 and 180 minutes: a control group without measuring ETTc pressure, and a study group with ETTc pressure measured and adjusted to a range 15-25 mmHg. The endoscopist was blinded to the study group allocation.

The mean ETTc pressure measured after estimation by palpation of the pilot balloon of the study group was 43 +/- 23.3 mm Hg before adjustment (the highest was 210 mm Hg), and 20+/- 3.1 mm Hg after adjustment (p< 0.001). The incidence of postprocedural sore throat, hoarseness, and blood-streaked expectoration in the control group was significantly higher than in the study group. As the duration of endotracheal intubation increased, the incidence of sore throat and blood-streaked expectoration in the control group increased. The incidence of sore throat in the study group also increased with increasing duration of endotracheal intubation. Fiberoptic bronchoscopy showed that the tracheal mucosa was injured in varying degrees in both groups, but the injury was more severe in the control group than in the study group.
So..time to get a cuff manometer for your ED or helicopter? Perhaps you already have one. What do you think?
Correlations Between Controlled Endotracheal Tube Cuff Pressure and Postprocedural Complications: A Multicenter Study
Anesth Analg. 2010 Nov;111(5):1133-7
Related posts:
Cuff pressure in flight
Paediatric cuff pressures

Better outcome with paediatric retrieval teams

Data from the England and Wales Paediatric Intensive Care Audit Network on children (aged 16 years or younger) admitted to 29 regional paediatric intensive care units (PICUs) between 1 January 2005 and 31 December 2008 were analysed in a retrospective cohort study to assess the effectiveness of the specialist retrieval teams.

The type of transferring team (specialist or non-specialist) was known for 16 875 cases and was specialist in 13 729 (81%). Compared with children transferred to PICUs from within the same hospital, children transferred from other hospitals were younger (median age 10 months vs 18 months), more acutely ill (mortality risk 6% vs 4% using the Paediatric Index of Mortality), needed more resources (such as invasive ventilation, vasoactive drugs, renal replacement therapy, extracorporeal membrane oxygenation and/or multiple-organ support), had longer stays in the PICU (median 75 h vs 43 h) and had a higher crude mortality (8% vs 6%). On multivariable analysis after adjustment for case mix and organisational factors, the risk of death among interhospital transfers was significantly (35%) lower than among intrahospital transfers. With similar analysis, the times spent in PICU did not differ significantly between these two groups. When the type of transferring team was considered, crude mortality was similar with specialist and non-specialist teams, although the children transferred by the specialist teams were more severely ill. On multivariable analysis, the risk of death was 42% lower with specialist team transfer.
These findings appear to confirm the value of specialist retrieval teams. Why children transferred from other hospitals did better than children transferred to the PICU in the same hospital is not explained.
Effect of specialist retrieval teams on outcomes in children admitted to paediatric intensive care units in England and Wales: a retrospective cohort study
Lancet. 2010 Aug 28;376(9742):698-704

Intubating spinal patients – the haemodynamics

Laryngoscopy and tracheal intubation transiently increase arterial pressure, heart rate (HR), and circulating catecholamines, in part attributed to reflex sympathetic discharge. In a complete spinal cord injury, the sympathetic nervous system and hence the cardiovascular responses to the intubation may be differentially affected according to the level of injury. Patients with acute quadriplegia often have a low resting arterial pressure due to inappropriate vasodilatation and loss of cardiac inotropy. Moreover, they frequently exhibit arrhythmias, reflex bradycardia, and cardiac arrest, especially during tracheal suction. In the days to weeks after injury, however, the reflex functioning of the lower cord recovers to maintain normal vascular tone. In the chronic stage, peripheral vascular changes and a loss of descending inhibitory control result in paroxysmal hypertension.
Korean investigators KY Yoo and colleagues1 aimed to determine the effect of the level (quadriplegia vs paraplegia) and duration of spinal cord injury on haemodynamic and catecholamine responses to laryngoscopy and tracheal intubation in patients with spinal cord injury. The outcome measures were the changes in systolic arterial pressure (SAP), HR, and catecholamine levels above awake baseline values after intubation.
Patients were divided into two groups: quadriplegia (above C7) and paraplegia (below T5). Each group was divided into six subgroups according to the time elapsed after the injury: <4 weeks (acute), 4 weeks– 1 yr, 1–5, 5–10, 10–20, and >20 yr. Twenty non-disabled patients undergoing surgery requiring tracheal intubation served as controls.
Patients with high-level paraplegia (T1–T4) were excluded because they were few in number and they had previously ‘shown different haemodynamic and catecholamine responses from the other groups2 which refers to work published by the same authors, in which high-paraplegic patients had a more pronounced increase in heart rate compared with other groups. Confusingly the ‘patients who were at increased risk of hyperkalemia after succinylcholine were excluded‘ although this statement appears only in the discussion, not the methods.
Anaesthesia was induced with sodium thiopental 5 mg/kg administered i.v. over 20 s, followed by succinylcholine 1 mg/kg for 5 s, and was followed by direct laryngoscopy and tracheal intubation.
Results were as follows:

  • SAP decreased after the induction of anaesthesia with thiopental in all subjects including the controls (P<0.05).
  • SAP then increased in response to tracheal intubation in the control and paraplegics (P<0.001), whereas it remained unaltered in the quadriplegics regardless of the time since injury.
  • In the paraplegics, the magnitude of maximum increase from baseline values was similar within 10 yr of injury, but was higher thereafter compared with that in the controls (P<0.05).
  • The maximum increase in SAP from baseline values after tracheal intubation was greater in the paraplegics than in the quadriplegics (P<0.0001).
  • An increase in SAP.130% of preinduction baseline values or 160 mm Hg was noted in three (4.2%) of 71 quadriplegics and 94 (65.7%) of 143 paraplegics.
  • The incidence of hypertension was significantly lower and that of hypotension significantly higher in the quadriplegics than in the control.
  • HR increased after induction ofanaesthesia in all groups, but less so in the quadriplegic groups.
  • Although baseline bradycardia was common in the acute quadriplegics, none of them showed further slowing during induction of anaesthesia and tracheal intubation.
  • Tracheal intubation increased plasma norepinephrine concentrations in all subjects except the acute quadriplegics.
  • Epinephrine concentrations were not significantly different between before and after intubation either in the quadriplegics or in the paraplegics, nor were they different between the groups with regard to the duration of injury.
  • The authors summarise: The pressor response was abolished in all quadriplegics regardless of the time elapsed after the injury. In contrast, the chronotropic and catecholamine responses differed over time. The chronotropic response was attenuated and the catecholamine response abolished in the acute quadriplegics. The chronotropic and catecholamine responses were improved in the quadriplegics after 4 weeks since the injury. In the paraplegic patients, cardiovascular responses did not change in the 10 yr after injury and the pressor response was enhanced at 10 yr or more after injury.
    1.Altered cardiovascular responses to tracheal intubation in patients with complete spinal cord injury: relation to time course and affected level
    Br J Anaesth. 2010 Dec;105(6):753-9
    2. Hemodynamic and catecholamine responses to laryngoscopy and tracheal intubation in patients with complete spinal cord injuries.
    Anesthesiolgy 2001; 95: 647–51

    Expert not happy with cricoid

    Evidence-based medicine reminds us to beware ‘experts’. However, here’s one self-described expert who talks some sense. Doctor (Doktor?) HJ Priebe from the University Hospital Freiburg in Germany suggests the risk of harm outweighs the risk of benefit from this procedure:
    Despite the lack of evidence for its effectiveness and evidence for numerous deleterious effects, cricoid pressure is still considered a standard of care during rapid sequence induction, and its application is considered mandatory in patients at high risk for gastric regurgitation. However, by using cricoid pressure, we may well be endangering more lives by causing airway problems than we are saving in the hope of preventing pulmonary aspiration. It is dangerous to consider cricoid pressure to be an effective and reliable measure in reducing the risk of pulmonary aspiration and to become complacent about the many factors that contribute to regurgitation and aspiration. Cricoid pressure is not a substitute for optimal patient preparation. Ensuring optimal positioning and a rapid onset of anesthesia and muscle relaxation to decrease the risk of coughing, straining or retching during the induction of anesthesia are likely more important in the prevention of pulmonary aspiration than cricoid pressure.

    ‘At the time of Sellick’s description of the technique of cricoid pressure, morbidity and mortality from pulmonary aspiration during the induction of anesthesia in the surgical population in general, and the obstetric population in particular, were of great concern. At that time, the concept of cricoid pressure was highly attractive. However, during the past 48 years, many aspects of anesthetic management have considerably changed, and knowledge has advanced. By today’s standards, cricoid pressure can no longer be considered an evidence-based practice. This is why more and more anesthetists (including myself) no longer apply cricoid pressure.

    Vielen Dank, Herr Doktor!
    Cricoid pressure: an expert’s opinion
    Minerva Anestesiol 2009;75:710-4 – Full text
    Just as well really, because these guys show many people don’t know how to do it anyway! Cases were identified in which pressure was mistakenly applied to the thyroid cartilage and even the sternocleidomastoid muscles!
    Variable application and misapplication of cricoid pressure
    J Trauma. 2010 Nov;69(5):1182-4