Category Archives: ICU

Stuff relevant to patients on ICU

All Updates, ICU, Resus, Trauma

Sedation for traumatic brain injury

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What are the best sedatives for patients with traumatic brain injury? A systematic review found no evidence that one sedative agent is better than another for improvement of neurologic outcome or mortality in critically ill adults with severe TBI. Thirteen randomised trials including around 380 patients were reviewed.
Why sedate brain injured patients anyway? Reasons include:

  • minimise noxious stimuli
  • improve patient comfort
  • reduce metabolic requirements of the injured brain to avoid ischemic progression of the traumatic lesion in presence of increased ICP
  • facilitate mechanical ventilation to control PaCo2
  • avoid ICP rises due to airway instrumentation such as those induced by coughing

Sedation generally improved intracranial pressure (ICP) and cerebral perfusion pressure (CPP) vs. baseline in most trials.
Interestingly boluses or short infusions of opioids resulted in (often transient) increases in ICP and decreases in MAP and CPP in three RCTs. An accompanying editorial suggests this may be due to large opioid doses (up to 3 μg/kg of fentanyl) and consequent hypotension; hypotension itself may trigger autoregulatory cerebral vasodilatation and increase ICP and decrease CPP. Although opioids have been linked with increased ICP through decreased cerebrovascular resistance, increased cerebral blood flow or Paco2, and disturbed cerebral autoregulation, they state that in studies in which hypotension after opioid administration was prevented, an ICP increasing effect was not seen. It is important to note the small sample sizes studied and the long time period of studies included, dating back some decades.
Importantly, ketamine did not result in the increase in ICP purported by older literature.


OBJECTIVES: To summarize randomized controlled trials on the effects of sedative agents on neurologic outcome, mortality, intracranial pressure, cerebral perfusion pressure, and adverse drug events in critically ill adults with severe traumatic brain injury.

DATA SOURCES: PubMed, MEDLINE, EMBASE, the Cochrane Database, Google Scholar, two clinical trials registries, personal files, and reference lists of included articles.

STUDY SELECTION: Randomized controlled trials of propofol, ketamine, etomidate, and agents from the opioid, benzodiazepine, α-2 agonist, and antipsychotic drug classes for management of adult intensive care unit patients with severe traumatic brain injury.

DATA EXTRACTION: In duplicate and independently, two investigators extracted data and evaluated methodologic quality and results.

DATA SYNTHESIS: Among 1,892 citations, 13 randomized controlled trials enrolling 380 patients met inclusion criteria. Long-term sedation (≥24 hrs) was addressed in six studies, whereas a bolus dose, short infusion, or doubling of plasma drug concentration was investigated in remaining trials. Most trials did not describe baseline traumatic brain injury prognostic factors or important cointerventions. Eight trials possibly or definitely concealed allocation and six were blinded. Insufficient data exist regarding the effects of sedative agents on neurologic outcome or mortality. Although their effects are likely transient, bolus doses of opioids may increase intracranial pressure and decrease cerebral perfusion pressure. In one study, a long-term infusion of propofol vs. morphine was associated with a reduced requirement for intracranial pressure-lowering cointerventions and a lower intracranial pressure on the third day. Trials of propofol vs. midazolam and ketamine vs. sufentanil found no difference between agents in intracranial pressure and cerebral perfusion pressure.

CONCLUSIONS: This systematic review found no convincing evidence that one sedative agent is more efficacious than another for improvement of patient-centered outcomes, intracranial pressure, or cerebral perfusion pressure in critically ill adults with severe traumatic brain injury. High bolus doses of opioids, however, have potentially deleterious effects on intracranial pressure and cerebral perfusion pressure. Adequately powered, high-quality, randomized controlled trials are urgently warranted.

Sedation for critically ill adults with severe traumatic brain injury: A systematic review of randomized controlled trials
Crit Care Med. 2011 Dec;39(12):2743-51

All Updates, ICU, Resus, Trauma

Predicting massive transfusion

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Do you have access to thromboelastometry in your Emergency Department? Further research by some of the first discoverers of acute traumatic coagulopathy involved using this tool to identify acute traumatic coagulopathy at 5 mins and predict the need for massive transfusion. Measures of coagulopathy more familiar to ED staff such as the INR took longer or (when point-of-care testing was employed) were less accurate.


OBJECTIVE: To identify an appropriate diagnostic tool for the early diagnosis of acute traumatic coagulopathy and validate this modality through prediction of transfusion requirements in trauma hemorrhage.

DESIGN: Prospective observational cohort study.

SETTING: Level 1 trauma center.

PATIENTS: Adult trauma patients who met the local criteria for full trauma team activation. Exclusion criteria included emergency department arrival >2 hrs after injury, >2000 mL of intravenous fluid before emergency department arrival, or transfer from another hospital.

INTERVENTIONS: None.

MEASUREMENTS: Blood was collected on arrival in the emergency department and analyzed with laboratory prothrombin time, point-of-care prothrombin time, and rotational thromboelastometry. Prothrombin time ratio was calculated and acute traumatic coagulopathy defined as laboratory prothrombin time ratio >1.2. Transfusion requirements were recorded for the first 12 hrs following admission.

MAIN RESULTS: Three hundred patients were included in the study. Laboratory prothrombin time results were available at a median of 78 (62-103) mins. Point-of-care prothrombin time ratio had reduced agreement with laboratory prothrombin time ratio in patients with acute traumatic coagulopathy, with 29% false-negative results. In acute traumatic coagulopathy, the rotational thromboelastometry clot amplitude at 5 mins was diminished by 42%, and this persisted throughout clot maturation. Rotational thromboelastometry clotting time was not significantly prolonged. Clot amplitude at a 5-min threshold of ≤35 mm had a detection rate of 77% for acute traumatic coagulopathy with a false-positive rate of 13%. Patients with clot amplitude at 5 mins ≤35 mm were more likely to receive red cell (46% vs. 17%, p < .001) and plasma (37% vs. 11%, p < .001) transfusions. The clot amplitude at 5 mins could identify patients who would require massive transfusion (detection rate of 71%, vs. 43% for prothrombin time ratio >1.2, p < .001).
CONCLUSIONS: In trauma hemorrhage, prothrombin time ratio is not rapidly available from the laboratory and point-of-care devices can be inaccurate. Acute traumatic coagulopathy is functionally characterized by a reduction in clot strength. With a threshold of clot amplitude at 5 mins of ≤35 mm, rotational thromboelastometry can identify acute traumatic coagulopathy at 5 mins and predict the need for massive transfusion.

Functional definition and characterization of acute traumatic coagulopathy.
Crit Care Med. 2011 Dec;39(12):2652-2658

Acute Med, All Updates, ICU, Resus

AF in sepsis and risk of stroke

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Atrial fibrillation can occur in the setting of severe sepsis, and often presents a therapeutic conundrum for critical care physicians, in that it can be relatively resistant to treatment until the sepsis has resolved, and its prognostic significance is unclear. A new study on a massive dataset shows atrial fibrillation in the setting of severe sepsis is associated with an increased risk of stroke and increased hospital mortality. Patients with severe sepsis who developed new-onset AF had a greater risk of in-hospital stroke than patients with preexisting AF and individuals without a history of AF.


Context New-onset atrial fibrillation (AF) has been reported in 6% to 20% of patients with severe sepsis. Chronic AF is a known risk factor for stroke and death, but the clinical significance of new-onset AF in the setting of severe sepsis is uncertain.

Objective To determine the in-hospital stroke and in-hospital mortality risks associated with new-onset AF in patients with severe sepsis.

Design and Setting Retrospective population-based cohort of California State Inpatient Database administrative claims data from nonfederal acute care hospitals for January 1 through December 31, 2007.

Patients Data were available for 3 144 787 hospitalized adults. Severe sepsis (n = 49 082 [1.56%]) was defined by validated International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) code 995.92. New-onset AF was defined as AF that occurred during the hospital stay, after excluding AF cases present at admission.

Main Outcome Measures A priori outcome measures were in-hospital ischemic stroke (ICD-9-CM codes 433, 434, or 436) and mortality.

Results Patients with severe sepsis were a mean age of 69 (SD, 16) years and 48% were women. New-onset AF occurred in 5.9% of patients with severe sepsis vs 0.65% of patients without severe sepsis (multivariable-adjusted odds ratio [OR], 6.82; 95% CI, 6.54-7.11; P < .001). Severe sepsis was present in 14% of all new-onset AF in hospitalized adults. Compared with severe sepsis patients without new-onset AF, patients with new-onset AF during severe sepsis had greater risks of in-hospital stroke (75/2896 [2.6%] vs 306/46 186 [0.6%] strokes; adjusted OR, 2.70; 95% CI, 2.05-3.57; P < .001) and in-hospital mortality (1629 [56%] vs 18 027 [39%] deaths; adjusted relative risk, 1.07; 95% CI, 1.04-1.11; P < .001). Findings were robust across 2 definitions of severe sepsis, multiple methods of addressing confounding, and multiple sensitivity analyses.
Conclusion Among patients with severe sepsis, patients with new-onset AF were at increased risk of in-hospital stroke and death compared with patients with no AF and patients with preexisting AF.

Incident Stroke and Mortality Associated With New-Onset Atrial Fibrillation in Patients Hospitalized With Severe Sepsis
JAMA. 2011 Nov 13. [Epub ahead of print]

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

2011 Asthma Guidelines

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The British Thoracic Society / SIGN Guidelines on asthma have been updated for 2011. There don’t seem to be any modificiations to the sections on acute severe asthma which were updated in 2009 and blogged here, although the treatment algorithms seem to be presented in a slightly different format and therefore are reproduced here:

Management of acute severe asthma in adults in hospital

Management of acute asthma in children in hospital

All Updates, ICU, PHARM, Resus

Preoxygenation and Prevention of Desaturation

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This paper is an excellent review article citing the cogent relevant evidence for optimal preoxygenation prior to RSI in the critically ill patient. The evidence has been interpreted with pertinent recommendations by two of the world’s heavy hitters in emergency medicine – Scott Weingart and Rich Levitan. If you can get a full text copy of the paper, laminate Figure 3 (‘Sequence of Preoxygenation and Prevention of Desaturation‘) and stick it to the wall in your resus bay!
The points covered include:

  • Why preoxygenate? Preoxygenation extends the duration of safe apnoea and should be considered mandatory, even in the crashing patient.
  • Standard non-rebreather facemasks set to the highest flow rate of oxygen possible should be used.
  • Allow 8 vital capacity breaths for co-operative patients or 3 minutes for everyone else.
  • Increasing mean airway pressure by CPAP/NIV or PEEP valves improves preoxygenation. However caution should be used in hypovolaemic shocked patients (decreased venous return) and should be reserved for patients who cannot preoxygenate >93-95% with high FiO2.
  • 20-degree head up or reverse Trendelenburg (in suspected trauma) improves pre oxygenation.
  • Apnoeic diffusion oxygenation can extend safe duration of apnoea after the RSI. Set nasal cannulae at 15L/min and leave on during intubation attempts. Ensure upper airway patency (ear to sternal notch and jaw thrust).
  • Active ventilation during onset of muscle relaxation should be assessed on a case by case basis and reserved for patients at high risk of desaturation (6-8 breaths per minute slowly, TV 6-7ml/kg).
  • If there is a high risk of desaturation rocuronium (1.2 mg/kg) may provide a longer duration of safe apnoea than suxamethonium with similar onset time.

Preoxygenation and Prevention of Desaturation During Emergency Airway Management
Ann Emerg Med. 2011 Nov 1. [Epub ahead of print]
[EXPAND Abstract]

Patients requiring emergency airway management are at great risk of hypoxemic hypoxia because of primary lung pathology, high metabolic demands, anemia, insufficient respiratory drive, and inability to protect their airway against aspiration. Tracheal intubation is often required before the complete information needed to assess the risk of periprocedural hypoxia is acquired, such as an arterial blood gas level, hemoglobin value, or even a chest radiograph. This article reviews preoxygenation and peri-intubation oxygenation techniques to minimize the risk of critical hypoxia and introduces a risk-stratification approach to emergency tracheal intubation. Techniques reviewed include positioning, preoxygenation and denitrogenation, positive end expiratory pressure devices, and passive apneic oxygenation.

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Acute Med, All Updates, ICU, Resus

Fluids contribute to acid-base disturbance on ICU

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Image from Wikipedia
I enjoyed a paper from Critical Care Medicine this month which relates to a major bugbear of mine: the prescription of 0.9% saline for critically ill patients and the consequent metabolic acidosis this causes. However it did produce some interesting findings that helped me review my own biases here.
In short, an ICU team decided to reduce and where possible eliminate the use of high chloride fluids including 0.9% saline and Gelofusine and replace with lower chloride fluids, mainly Ringer’s Lactate (Hartmann’s solution).
It is known that saline causes a metabolic acidosis by elevating chloride and reducing the strong ion difference. This results in a normal anion gap, hyperchloraemic acidosis. The clinical significance of this is uncertain, but the iatrogenic acidosis is often confused by clinicians as a sign of severe illness, especially those clinicians that don’t look at the chloride or anion gap.
Not surprisingly, changing the fluid policy resulted in less acidosis (and also less hypernatraemia). There was however an increase in severe alkalaemia. The study was not designed to look at patient oriented outcomes.
My observations are:

  • This is an important reminder that saline causes acidosis
  • Because of the possibility of worsening alkalosis, fluid therapy choice should be individualised for an ICU patient based on their known acid-base issues; in some cases, saline may be appropriate.
  • These patients were managed for several days on an ICU. Alkalaemia is common on the ICU for reasons that include hypoalbuminaemia, furosemide use, and iatrogenic hyperventilation. These factors are less relevant in the ED resuscitation population where such a degree of alkalaemia is rarely seen.
  • The authors point out that their results are “consistent with previous acute treatment studies, which were conducted in the perioperative or experimental setting” – isn’t it a shame that ED-based studies are not forthcoming?

The authors point to an additional finding:


Furthermore, our results suggest that routine use of lactate fluids such as Hartmann’s or Ringer’s lactate is associated with a detectable iatrogenic increase in lactate in the first 48 hrs after ICU admission, when, presumably, lactate clearance is less effective.

While this is interesting, the mean [SD] lactate values in the two groups were 1.79 [1.57] and 2.05 [1.61] so while statistically significant I suspect this is clinically irrelevant. And as we know, the cause of a raised lactate is more of a concern than the fact of a raised lactate
A significant benefit of the change in fluid policy was a signficant cost saving, largely due to the omission of Gelofusine.
For me, this study reassures me that my current practice of preferring Ringer’s Lactate to Saline in the resuscitation setting is likely to minimise iatrogenic acidosis without significantly elevating the lactate, in a population rarely afflicted by significant alkalaemia.
The biochemical effects of restricting chloride-rich fluids in intensive care
Crit Care Med. 2011 Nov;39(11):2419-2424
[EXPAND Abstract]


Objective: To determine the biochemical effects of restricting the use of chloride-rich intravenous fluids in critically ill patients.

Design: Prospective, open-label, before-and-after study.

Setting: University-affiliated intensive care unit.

Patients: A cohort of 828 consecutive patients admitted over 6 months from February 2008 and cohort of 816 consecutive patients admitted over 6 months from February 2009.

Interventions: We collected biochemical and fluid use data during standard practice without clinician awareness. After a 6-month period of education and preparation, we restricted the use of chloride-rich fluids (0.9% saline [Baxter, Sydney, Australia], Gelofusine [BBraun, Melsungen, Germany], and Albumex 4 [CSL Bioplasma, Melbourne, Australia]) in the intensive care unit and made them available only on specific intensive care unit specialist prescription.

Measurements and Main Results: Saline prescription decreased from 2411 L in the control group to 52 L in the intervention group (p < .001), Gelofusine from 538 to 0 L (p < .001), and Albumex 4 from 269 to 80 L (p < .001). As expected, Hartmann’s lactated solution prescription increased from 469 to 3205 L (p < .001), Plasma-Lyte from 65 to 160 L (p < .05), and chloride-poor Albumex 20 from 87 to 268 L (p < .001). After intervention, the incidence of severe metabolic acidosis (standard base excess5 mEq/L) and alkalemia (pH >7.5) with an increase from 25.4% to 32.8% and 10.5% to 14.7%, respectively (p < .001). The time-weighted mean chloride level decreased from 104.9 ± 4.9 to 102.5 ± 4.6 mmol/L (p < .001), whereas the time-weighted mean standard base excess increased from 0.5 ± 4.5 to 1.8 ± 4.7 mmol/L (p < .001), mean bicarbonate from 25.3 ± 4.0 to 26.4 ± 4.1 mmol/L (p < .001) and mean pH from 7.40 ± 0.06 to 7.42 ± 0.06 (p < .001). Overall fluid costs decreased from $15,077 (U.S.) to $3,915.

Conclusions: In a tertiary intensive care unit in Australia, restricting the use of chloride-rich fluids significantly affected electrolyte and acid-base status. The choice of fluids significantly modulates acid-base status in critically ill patients.

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Acute Med, All Updates, ICU, PHARM, Resus

咽反射是沒用的 – just as we thought

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The painful dogma of “GCS ≤8 = intubate” is nicely challenged by the A&E Academic Unit at Prince of Wales Hospital in Hong Kong, who provide some further evidence that patients with a higher GCS may have absent airway protective reflexes, and patients with a lower GCS may have intact reflexes.


AIM: To describe the relationship of gag and cough reflexes to Glasgow coma score (GCS) in Chinese adults requiring critical care.

METHOD: Prospective observational study of adult patients requiring treatment in the trauma or resuscitation rooms of the Emergency Department, Prince of Wales Hospital, Hong Kong. A long cotton bud to stimulate the posterior pharyngeal wall (gag reflex) and a soft tracheal suction catheter were introduced through the mouth to stimulate the laryngopharynx and elicit the cough reflex. Reflexes were classified as normal, attenuated or absent.

RESULTS: A total of 208 patients were recruited. Reduced gag and cough reflexes were found to be significantly related to reduced GCS (p=0.014 and 0.002, respectively). Of 33 patients with a GCS≤8, 12 (36.4%) had normal gag reflexes and 8 (24.2%) had normal cough reflexes. 23/62 (37.1%) patients with a GCS of 9-14 had absent gag reflexes, and 27 (43.5%) had absent cough reflexes. In patients with a normal GCS, 22.1% (25/113) had absent gag reflexes and 25.7% (29) had absent cough reflexes.

CONCLUSIONS: Our study has shown that in a Chinese population with a wide range of critical illness (but little trauma or intoxication), reduced GCS is significantly related to gag and cough reflexes. However, a considerable proportion of patients with a GCS≤8 have intact airway reflexes and may be capable of maintaining their own airway, whilst many patients with a GCS>8 have impaired airway reflexes and may be at risk of aspiration. This has important implications for airway management decisions.

What is the relationship between the Glasgow coma scale and airway protective reflexes in the Chinese population?
Resuscitation. 2011 Jul 23. [Epub ahead of print]
Related post: Do all comatose patients need intubation?

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

Oxygen therapy for asthma can elevate CO2

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Patients with acute exacerbations of asthma randomised to receive high concentration oxygen therapy showed a greater rise in CO2 than those who received titrated oxygen to keep SpO2 > 93%.
This study has a few weaknesses but raises an interesting challenge to the dogma of high flow oxygen (and oxygen driven nebulisers) for all acute asthma exacerbations.
The suggested main mechanism for the elevation in CO2 is worsening ventilation/perfusion mismatching as a result of the release of hypoxic pulmonary vasoconstriction and a consequent increase in physiological dead space. The authors remind us that this has been demonstrated in other studies on asthma and acute COPD exacerbations. The authors infer that high concentration oxygen therapy may therefore potentially increase the PaCO2 across a range of respiratory conditions with abnormal gas exchange due to ventilation/perfusion mismatching
Some of the weaknesses include lack of blinding, recruiting fewer patients than planned, and changing their primary outcome variable after commencing the study (which the authors are honest about) from absolute CO2 to increase in CO2 (since it was apparent on preliminary analysis of the first few patients that presenting CO2 was the primary determinant of subsequent CO2). Furthermore, the CO2 was measured from a transcutaneous device as opposed to the true ‘gold standard’ of arterial blood gas analysis, although good reasons are given for this.
Despite some of these drawbacks this study provides us with a further reminder that oxygen is a drug with some unwanted effects and therefore its dose needs to be individualised for the patient.


Background The effect on Paco(2) of high concentration oxygen therapy when administered to patients with severe exacerbations of asthma is uncertain.

Methods 106 patients with severe exacerbations of asthma presenting to the Emergency Department were randomised to high concentration oxygen (8 l/min via medium concentration mask) or titrated oxygen (to achieve oxygen saturations between 93% and 95%) for 60 min. Patients with chronic obstructive pulmonary disease or disorders associated with hypercapnic respiratory failure were excluded. The transcutaneous partial pressure of carbon dioxide (Ptco(2)) was measured at 0, 20, 40 and 60 min. The primary outcome variable was the proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min.

Results The proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min was significantly higher in the high concentration oxygen group, 22/50 (44%) vs 10/53 (19%), RR 2.3 (95% CI 1.2 to 4.4, p<0.006). The high concentration group had a higher proportion of patients with a rise in Ptco(2) ≥8 mm Hg, 11/50 (22%) vs 3/53 (6%), RR 3.9 (95% CI 1.2 to 13.1, p=0.016). All 10 patients with a final Ptco(2) ≥45 mm Hg received high concentration oxygen therapy, and in five there was an increase in Ptco(2) ≥10 mm Hg.
Conclusion High concentration oxygen therapy causes a clinically significant increase in Ptco(2) in patients presenting with severe exacerbations of asthma. A titrated oxygen regime is recommended in the treatment of severe asthma, in which oxygen is administered only to patients with hypoxaemia, in a dose that relieves hypoxaemia without causing hyperoxaemia.

Randomised controlled trial of high concentration versus titrated oxygen therapy in severe exacerbations of asthma
Thorax. 2011 Nov;66(11):937-41

Acute Med, All Updates, ICU, Resus

Xigris withdrawn

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Pharmaceutical company Eli Lilly has announced the withdrawal of its severe sepsis drug activated protein C, or drotrecogin alfa (proprietary name Xigris). This is because the PROWESS-SHOCK study, now complete, showed no benefit in its primary endpoint of 28 day mortality when compared with placebo in septic shock patients. There was also no benefit in a subgroup of patients with protein C deficiency, and no significant increased risk of severe bleeding.
The European Medicines Agency’s Instructions are:


At this stage physicians should not initiate treatment with Xigris in new patients and should stop ongoing treatment

The US Food and Drug Administration’s Instructions are:


Xigris treatment should not be started in new patients. Xigris treatment should be stopped in patients being treated with Xigris.

All remaining Xigris product should be returned to the supplier from whom it was purchased.

The UK Intensive Care Society’s Announcement contains a link to Eli Lilly’s press release.

The Xigris website looks like this at the time of posting
Acute Med, All Updates, ICU, Resus

'Cryptic shock' important but not always very cryptic

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Patients with severe sepsis and an elevated lactate who appear to be normotensive had a mortality similar to those presenting with hypotension. This is demonstrated in a new study on patients who were recruited to a study I have reported before.
The so-called ‘cryptic shock’ group was defined by a systolic BP of at least 90 mmHg, suggesting to me not so much that normotension and hypotension are prognostically equivalent, but that we should perhaps redefine hypotension in sepsis, as we should probably be doing in trauma. Alternatively (and preferably), the BP should be interpreted in the context of what is known to be or likely to be normal for that patient. For example, a systolic BP of 105 mmHg in a 75 year old male would be be ringing serious alarm bells for me in a febrile patient, and I would be working them up for severe sepsis from the start. Interestingly in this study, the cryptic shock group had a higher proportion of patients with diabetes and/or end stage renal disease – diagnoses one would expect to be associated with hypertension – and the median (and IQR) systolic BP in this group was 108 (92, 126). So, although this shock may have been ‘cryptic’ as opposed to ‘overt’ by the definition applied in the paper (a cut off of 90 mmHg), it is likely that some of the patients in the cryptic group were hypotensive compared with their usual blood pressure.
These observations do not detract from a key message the authors include in their discussion, with which I wholeheartedly agree:
“These data highlight the need to screen patients for signs of occult hypoperfusion, and given the high mortality rate associated with an elevated serum lactate, also suggest that patients with biochemical evidence of inadequate oxygen delivery despite normal blood pressure should be included in early sepsis resuscitation pathways.”
This paper makes an important contribution to the sepsis literature by warning against the dismissal of an elevated serum lactate in the setting of apparent haemodynamic stability as being a less acutely ill patient than one presenting with overt hypotension. It provides a reminder to check the lactate in patients with infection and signs of systemic inflammatory response, since this may provide the only early evidence of hypoperfusion.

Outcomes of patients undergoing early sepsis resuscitation for cryptic shock compared with overt shock
Resuscitation. 2011 Oct;82(10):1289-1293
[EXPAND Click to read abstract]


Introduction We sought to compare the outcomes of patients with cryptic versus overt shock treated with an emergency department (ED) based early sepsis resuscitation protocol.

Methods Pre-planned secondary analysis of a large, multicenter ED-based randomized controlled trial of early sepsis resuscitation. All subjects were treated with a quantitative resuscitation protocol in the ED targeting 3 physiological variables: central venous pressure, mean arterial pressure and either central venous oxygen saturation or lactate clearance. The study protocol was continued until all endpoints were achieved or a maximum of 6 h. Outcomes data of patients who were enrolled with a lactate ≥4 mmol/L and normotension (cryptic shock) were compared to those enrolled with sustained hypotension after fluid challenge (overt shock). The primary outcome was in-hospital mortality.

Results A total of 300 subjects were enrolled, 53 in the cryptic shock group and 247 in the overt shock group. The demographics and baseline characteristics were similar between the groups. The primary endpoint of in-hospital mortality was observed in 11/53 (20%, 95% CI 11–34) in the cryptic shock group and 48/247 (19%, 95% CI 15–25) in the overt shock group, difference of 1% (95% CI −10 to 14; log rank test p = 0.81).

Conclusion Severe sepsis with cryptic shock carries a mortality rate not significantly different from that of overt septic shock. These data suggest the need for early aggressive screening for and treatment of patients with an elevated serum lactate in the absence of hypotension.

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