Investigations
1st investigations to order
lactate (from arterial blood gas)
Test
Shock is present if level >2 mmol/L (>18 mg/dL).[1][3]
Perform serial measurements if the lactate is >2 mmol/L (>18 mg/dL).
Frequency of repeat testing depends on cause of shock and treatment given.
Increased serum lactate was previously thought to indicate tissue hypoperfusion, decreased tissue oxygenation, and anaerobic metabolism.[25] More recently, this is being challenged by the view that lactate is elevated due to the stress response as anaerobic metabolism is a pre-terminal event.[32]
Practical tip
Involve senior support if lactate levels remain persistently >4 mmol/L (>36 mg/dL) as this indicates a high risk of death.[25]
Evidence: Measurement of lactate
Use serial measurement of lactate to guide resuscitation.
Five randomised controlled trials (647 patients) have evaluated lactate-guided resuscitation of patients with septic shock.[80][81][82][83][84] They showed a significant reduction in mortality in lactate-guided resuscitation compared with resuscitation without lactate monitoring. Two other meta-analyses of the 647 patients who were enrolled in these trials demonstrated moderate evidence for reduction in mortality when an early lactate clearance strategy was used, compared with either usual care or with treatment guided by central venous oxygen saturation (ScvO2) measurement.[85][86]
Evidence has also shown the value of serial lactate measurements for predicting prognosis.
One prospective study identified 76 patients with hypovolaemic shock and showed that changes in lactate concentrations provide an early and objective evaluation of a patient's response to therapy. It suggested that repeated lactate determinations represent a reliable prognostic index for patients with circulatory shock.[87]
Another observational study in patients with shock secondary to multiple trauma evaluated the correlation between lactate clearance and survival. All patients in whom lactate levels returned to the normal range (≤2 mmol/L [≤18 mg/dL]) within 24 hours survived. Survival decreased to 77.8% if normalisation occurred within 48 hours and to 13.6% in those patients in whom lactate levels were elevated above 2 mmol/L (18 mg/dL) for more than 48 hours.[88]
Result
>2 mmol/L (>18 mg/dL).
venous blood gas (VBG) or arterial blood gas (ABG)
Test
Use to detect metabolic acidosis with a high lactate and negative base excess, most commonly present in shock.[25][37]
VBG is increasingly being used as it is less invasive and painful.
Evidence suggests that venous pH has sufficient agreement with arterial pH for it to be an acceptable alternative in clinical practice for most patients
Evidence: Base deficit as a prognostic marker
The initial base deficit on ABG is a good independent predictor of mortality in patients with haemorrhagic shock.
One study stratified the extent of base deficit into three categories of mild (-3 to -5 mEq/L), moderate (-6 to -9 mEq/L), and severe (<-10 mEq/L) and found a significant correlation between the admission base deficit and transfusion or fluid requirements within the first 24 hours and the risk of organ failure or death.[89]
The base deficit is a better prognostic marker of death than the pH in arterial blood gas analyses.[90]
Furthermore, the base deficit represents a highly sensitive marker for the extent of shock and mortality, both in adult and paediatric patients.[91][92]
Result
Metabolic acidosis: pH <7.35, bicarbonate <22.
glucose
Test
May be increased due to stress response initiated due to shock.[32]
May be increased in other causes such as diabetic ketoacidosis.[33]
Evidence: Hyperglycaemia is a response to critical illness
Stress hyperglycaemia and insulin resistance are evolutionarily preserved responses that allow the host to survive during periods of severe stress.[32]
In animal models of haemorrhagic shock the administration of hypertonic glucose solution increased cardiac output and blood pressure, and improved survival.
In these experiments, similar osmolar doses of saline or mannitol, with greater accompanying fluid volumes, failed to produce the sustained blood pressure changes or to improve the survival.[93]
Result
>7 mmol/L (>126 mg/dL) is abnormal in a non-diabetic patient.
full blood count
Test
May support diagnosis of underlying cause.
Hb may be decreased with acute bleeding.[39][94]
Hb <100 g/L (<10 g/dL) is suggestive of haemorrhage as the cause; however, it may be normal in the early stages due to vasoconstriction.
Practical tip
Haemoglobin does not immediately fall in acute blood loss. Therefore, do not be falsely reassured with a normal Hb, especially if the blood sample has been taken early.
WBC count may be elevated with infection or inflammation.[24]
Result
Hb <100 g/L (<10 g/dL) suggests haemorrhage as the cause; however, may be normal in the early stages due to vasoconstriction.
WBC count may be >12 x 10³/microlitre if sepsis is present.
urea and electrolytes
Test
These may be deranged due to the underlying cause or as a result of renal hypoperfusion.[95]
Urea and creatinine may be raised in renal hypoperfusion. Urea may be disproportionately raised with upper gastrointestinal bleeding, dehydration, or cardiac failure.[48]
Electrolytes may be deranged depending on the cause of shock.
Result
Evidence of renal impairment if kidney perfusion is compromised.[95]
Urea disproportionately raised with upper gastrointestinal bleeding, dehydration, or cardiac failure.[48][95]
Hyperkalaemia in trauma, acute kidney injury, and diabetic ketoacidosis.[33][95]
Hypokalaemia with diarrhoea or vomiting.[95]
Hypernatraemia in burns and diarrhoea or vomiting.[95]
Hyponatraemia in trauma and also sometimes in diarrhoea and vomiting.[95]
coagulation studies
Test
Include prothrombin time (PT), activated PTT, and fibrinogen.[39][94]
Baseline test especially prior to central venous catheter insertion.[2]
May also be deranged in patients with trauma and is a predictor of mortality.[38]
May also be deranged in disseminated intravascular coagulation secondary to sepsis.
Evidence: Coagulopathy is common in trauma patients with shock
The incidence of coagulation abnormalities, early after trauma, is high, and they are independent predictors of mortality even in the presence of other risk factors.
One study prospectively collected data on trauma patients presenting to a level 1 trauma centre. A logistic regression analysis was performed of PT, PTT, platelet count, and confounders to determine whether coagulopathy is a predictor of all-cause mortality. An initial abnormal PT increased the adjusted odds of dying by 35% and an initial abnormal PTT increased the adjusted odds of dying by 326%.[38]
Result
May be prolonged (e.g., disseminated intravascular coagulation associated with septic shock).
C-reactive protein
Test
High CRP levels (>1904.8 nanomol/L [>200 mg/L]) indicate severe inflammation.
The higher the level, the greater the degree of inflammation.
Lower concentrations (<1904.8 nanomol/L [<200 mg/L]) may be found in septic states but also after myocardial infarction or surgery.
Result
High values suggest infection and inflammation; consider sepsis as a cause.
procalcitonin
Test
Elevated procalcitonin levels have been associated with sepsis and may help differentiate sepsis from causes of the systemic inflammatory response syndrome.[96][97]
High procalcitonin levels are associated with mortality from sepsis in 90-day follow-up.
Other pro-inflammatory states, such as acute pancreatitis, trauma, major surgery, and burns, can also increase procalcitonin.[98]
Changes in procalcitonin levels may occur later than that of lactate, although changes in both markers combined are highly predictive of outcome between 24 to 48 hours.[99]
Result
High values suggest sepsis.
ECG
Test
May show the underlying cause of shock.[3][14][29][36]
Consider repeat ECGs or continuous monitoring of the ECG trace if critically unwell.
Ensure all patients with cardiogenic shock have continuous cardiac monitoring.[14]
Result
Evidence of myocardial ischaemia in cardiogenic shock.
Arrhythmia (e.g., atrial fibrillation, bradyarrhythmias).
Evidence of right heart strain in massive pulmonary embolism.
Evidence of underlying electrolyte abnormalities (e.g., hypokalaemia or hyperkalaemia).
Investigations to consider
chest x-ray
Test
May show the underlying cause of shock.[37][103]
Do not use for tension pneumothorax - urgent decompression is the first line intervention.
Result
Consolidation in sepsis secondary to pneumonia.
Pleural effusion in acute heart failure secondary to myocardial infarction.
Pneumothorax.
Pulmonary infarction secondary to pulmonary embolism.
Widened mediastinum with aortic dissection.
urinalysis and urine pregnancy test
Test
Look for signs of infection in suspected sepsis.
Perform in all women of childbearing age to detect ectopic pregnancy.
Result
Positive beta human chorionic gonadotrophin in ectopic pregnancy.
Signs of infection include blood, nitrites, and leukocytes.
Ketones may be present in diabetic ketoacidosis or vomiting and diarrhoea.
infection screen
Test
Order if there is suspicion of infection, especially in sepsis. Decide on which tests to order based on source of infection suspected. Specific tests include:
Blood cultures
Respiratory swabs for polymerase chain reaction
Sputum, urine, cerebrospinal fluid, or wound samples for microscopy, culture, and sensitivity.
Result
Evidence of infection.
point-of-care ultrasound
Test
This is a useful bedside test to identify the underlying cause of shock.
This should only be performed by a senior doctor with specialist ultrasound training.
Follow a protocol such as Rapid Ultrasound in Shock (RUSH).[104]
RUSH involves assessing the lungs, inferior vena cava (IVC), abdominal aorta, and abdomen.
Use echocardiography to assess cardiac function.[14]
Perform this in all patients with cardiogenic shock and undifferentiated shock. There is no benefit to performing this in patients with haemorrhagic, anaphylactic, or neurogenic shock.
Do not routinely use in patients where the cause of shock is clear and who are responding to initial treatment.[2]
Use to:
Identify cause of shock if not clear on initial assessment.
Select the most appropriate treatment
Use to evaluate cardiac output and stroke volume to determine whether inotropes are needed.
Assess response to treatment
Use to assess fluid responsiveness: defined as an increase of stroke volume of 10% to 15% after the patient receives 500 mL of crystalloid over 10-15 minutes.
Use Focused Assessment with Sonography for Trauma (FAST) scan for patients with trauma to look for free fluid.[18]
Result
Lungs: B-lines suggest pulmonary oedema; lung sliding suggests pneumothorax.
Cardiac function: left ventricular failure suggests myocardial infarction; right ventricular strain suggests pulmonary embolism; pericardial effusion suggests cardiac tamponade.
IVC: compressibility suggests the patient needs more fluid; non-compressibility suggests the patient will not respond to more fluid.
Abdominal aorta: abdominal aortic aneurysm.
Abdomen: ectopic pregnancy.
Obstructed biliary or renal tracts.
CT chest, abdomen, and pelvis
Test
Use especially in patients with major trauma. Other indications may include suspected ruptured aortic aneurysm or intra-abdominal collection.[31]
Potentially unsafe in a haemodynamically unstable patient. Patients must be stable before transfer to the imaging suite.
Result
May show underlying cause such as bleeding, ruptured aortic aneurysm, or intra-abdominal collection.
computed tomographic pulmonary angiography (CTPA)
Test
If you suspect pulmonary embolism (PE), use CTPA (if indicated) alongside other appropriate assessment tools.[106][107]
CTPA is the preferred investigation for definitive confirmation of PE; it is appropriate to use CTPA in most (but not all) patients.[106]
See Pulmonary embolism.
Result
PE is confirmed by direct visualisation of thrombus in a pulmonary artery; appears as a partial or complete intraluminal filling defect.
x-ray long bones
Test
Fractures of the femur can cause shock due to blood loss, especially in older people.
Result
Fractures of long bones.
x-ray spine
Test
Perform where there is suspicion of spinal injury in cases of neurogenic shock.
Result
Fracture of spine.
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