202501041555
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Tags: Trauma
Abdominal trauma
Acute traumatic coagulopathy (ATC) describes the phenomenon of direct shock-induced haemostatic deficit.
Acute traumatic coagulopathy appears to be driven initially by severe tissue damage, shock-related hypoperfusion and an inflammatory response leading to the activation of anticoagulant pathways, fibrinolytic pathways and platelet dysfunction
Trauma-induced coagulopathy (TIC) describes the multifactorial coagulopathy associated with trauma including ATC plus dilution, hypothermia, acidosis and other factors
Trauma-induced coagulopathy develops in around one-third of patients with traumatic bleeding; its incidence correlates with increasing severity of injury
The first step in rehabilitation from trauma (returning an individual to their functional state before the injury) is the acute resuscitative phase where the objectives are to
- prevent deterioration,
- restore physiological homeostasis,
- prevent death
- ultimately restore anatomy and function.
The central components of DCR (damage control resus) are:
Certain characteristics have been proposed to identify patients who may benefit from DCR:
- hypotension
- systolic BP <90 mmHg
- <110 mmHg in those aged >65 yrs
- shock index (heart rate divided by systolic BP) >1
- serum lactate >2.5 mmol/L
- base deficit >–6
- abnormal INR or VHA
- +ve FAST
Damage-control surgery
originally defined as ‘initial control of haemorrhage and contamination followed by intraperitoneal packing and rapid closure’ to facilitate restoration of physiology in the ICU and later definitive surgery
For control of haemorrhage, surgical manoeuvres may include
- packing (liver and pelvic injuries);
- removal of injured viscera (spleen or kidney);
- ligation, repair or temporary shunting of vascular injuries
Reperfusion syndrome including vasoplegia, arrhythmias and hyperkalaemia may be encountered after restoration of flow such as release of clamps, repair of vessels or deflation of REBOA
Control of contamination may involve drainage in biliary, duodenal or pancreatic injury, stapled resection of injured gastrointestinal segments, and deferring of anastomosis or stoma
Temporary abdominal closure is common and facilitates easy re-entry, preservation of fascia for later definitive closure and reduces the likelihood of abdominal compartment syndrome
Elements of DCS
Indications
- Presence of shock or other elements of the lethal triad unresponsive to resuscitation indicating a lack of physiological reserve to tolerate a lengthier definitive procedure
- Inability to obtain definitive haemostasis and temporising measures such as packing must remain in situ
- Complex injury patterns including multiple penetrating, combined vascular/visceral, multicompartment or high-energy blunt injuries. In these patients:
- Bleeding may be from multiple sites requiring effective prioritisation, or at locations predisposed to rebleeding or poorly visualised
- Definitive surgery would require a lengthy operative time
Aims:
- Control haemorrhage
- Control pulmonary air leak
- Control bowel content
- Reperfuse critical organs and limbs
Usual process: - Abbreviated initial surgery to achieve above goals alongside concurrent ongoing damage-control resuscitation
- A period of physiological recovery and ongoing resuscitation in the ICU
- Return to operating theatre for initial relook, definitive repair and closure when possible
- When needed, a further return for abdominal wall closure
Definitive repair is undertaken after correction of shock, acidosis, hypothermia, coagulopathy and anaemia, occurring 24–48 h later depending on the patient's condition and organisational capacity
Multiple repeat laparotomies may be required. About 30–60% of patients cannot be closed at this time because of visceral oedema and fascial retraction, requiring a subsequent procedure
Permissive hypotension
In the patient in haemorrhagic shock with a significantly ↓ circulating volume, relatively small volumes of crystalloid or colloid solutions can cause significant haemodilution
current evidence suggests that permissive hypotension is safe and confers a mortality benefit alongside ↓ in blood loss and usage
Hypotension is not a therapeutic target in itself but, for example, the literature describes the acceptance of
- MAP of 50 mmHg
- SBP of 70 mmHg
Increasing SVR, although improving arterial pressure, is often counterproductive to resuscitation targets as increased arterial pressure correlates with increased bleeding and risks destabilising newly formed clot, and therefore vasopressor drugs are generally avoided
When bleeding is ongoing, attempts to use volume resuscitation to restore preload, cardiac output, perfusion and thus BP are futile, may increase bleeding because of higher venous pressure, and result in large volumes infused with little benefit. This is classically described as the transient- or non-responder
patients who can sustain, for example, a MAP of 65 mmHg after volume resuscitation without vasopressors, are unlikely to be actively bleeding and BP and perfusion can be managed as per the anaesthetist's usual practice
Inevitably present are the dilutional effects of even balanced blood product use and the inflammatory effects of allogenic blood transfusion, in addition to an increased risk of post-injury infection and multiorgan failure, and the usage of a precious resource
The tolerated duration of permissive hypotension is often quoted as 1 h, as animal models show that the physiological deterioration and metabolic acidosis caused by tissue hypotension are still reversible with a return to normotensive resuscitation by this time
Hypotension is harmful in TBI, but haemorrhage control takes precedence as the end point of uncontrolled haemorrhage will be death regardless of the neurological status.
Blood product resuscitation
early use of PRBCs and FFP, followed by later addition of platelets and cryoprecipitate as a replacement source of fibrinogen
Fresh frozen plasma is given in a 1:1 ratio with PRBCs so as not to worsen TIC by causing a dilutional coagulopathy
TXA is given using an initial bolus of 1 g, followed by a subsequent 1 g infusion over 8 h
Major trials:
PROPPR
1:1 PRBCs and FFP ratio use reduces death from exsanguination, but not overall mortality in 24 h, without an increase in transfusion-related complications
PROCOAG
Four-factor prothrombin complex concentrate does not decrease 24-h blood product consumption and causes an increase in thromboembolic complications
CRYOSTAT-2
Early empirical high-dose cryoprecipitate does not reduce 28-day mortality
CRASH-2
Tranexamic acid reduces mortality in trauma if given within 3 h
Hypothermia adversely affects coagulation by causing
- enzyme dysfunction,
- platelet dysfunction,
- ↑ fibrinolysis
Blood gas analysis should be performed frequently (e.g. Q15 min) during resuscitation
Hyperkalaemia becomes increasingly common as transfusion ensues, probably because of the potassium content of PRBCs and its release from damaged and ischaemic tissues
Calcium plays an important role in trauma, mitigating the effects of potassium on cardiac conduction and contractility. It also has critical roles in vascular tone, and haemostasis including on platelet activation and adhesion, and as an enzyme cofactor
Paradoxically, the acidosis associated with shock causes displacement of calcium from albumin and increases free ionised calcium concentrations, but this is not enough to mitigate loss and maldistribution.
Haemodynamic effects are apparent at serum Ca2+ concentrations <0.8 mmol/L and effects on clotting at concentrations <0.56 mmol/L
Approximately 10 mmol calcium chloride is needed for every 4–6 units of PRBCs.
No good evidence supporting use of NaHCO3
Tris-hydroxymethyl amino methane (THAM) is an alternative buffer that may avoid these issues but is not currently used in the UK
VHA:
iTACTIC study reported no improvement in patients alive and free of massive transfusion at 24 h with VHA compared with fixed-ratio therapy guided by conventional coagulation tests (CCTs). Conversely, other studies have shown benefit, with decreased mortality and massive transfusion rate at 24 h, decreased use of blood components and decreased costs with VHA
Pre-op / at A&E
based on ATLS
The roles of the anaesthetist include
- confirming adequacy of airway and breathing,
- ensuring the airway is secured as necessary,
- assisting with vascular access,
- carefully using sedative drugs if appropriate in patients whose trachea is already intubated or giving analgesic drugs in non-intubated patients,
- preparing for expedient onward transfer for imaging or intervention
Induction of anaesthesia is usually best deferred to the operating theatre
Venous access should be high-flow and above the diaphragm because the continuity of the vasculature with the heart may be disrupted below this in trauma
Clinicians should be aware that certain conditions may mimic the physiological presentation of haemorrhage including cardiac tamponade, TBI and spinal cord injury, whereas the catecholamine response will compensate for and obscure evidence of bleeding, particularly in young and healthy patients.
CT vs IR vs OT
The hallmark of an effective surgical pathway is the ability to bypass CT and make use of this time in the operating theatre for patients who are haemorrhaging and in extremis
All the major locations of bleeding (chest, abdomen, pelvis, retroperitoneum and external haemorrhage) can be definitively explored operatively, with capacity to immediately intervene.
In addition to identifying bleeding sources and concurrent injury including brain and spinal cord trauma, CT can also identify pathology potentially amenable to angioembolisation
Abdominal injuries amenable to an IR-only strategy include active arterial pelvic or solid organ (spleen, liver or kidney) haemorrhage. Arterial haemorrhage that involves junctional or challenging surgical locations may be amenable to a joint IR/surgery approach
Exploratory laparotomy remains the gold standard for patients with
- peritonitis,
- evisceration,
- a penetrating object in situ,
- diaphragmatic injury,
- clinical or CT suggestion of hollow viscus injury
Contrast-enhanced CT of the chest, abdomen and pelvis is the definitive modality in this patient group, with non-contrast head and neck, and arterial-phase neck and limb imaging as indicated by the pattern of injury
BASTE mnemonics
- blood (review situation and future need),
- acid/base (pH and lactate status),
- surgical progress,
- temperature,
- electrolytes (potassium and calcium)
Intra-op
Preparation
Equipment
- Operating bed with two arm boards in crucifix position
- Laparotomy, thoracotomy, chest drain, tourniquet equipment
- Warming: maximise ambient temperature, forced air warmer, warming mattress
- Rapid infuser prepared and connected to patient before induction
- Paperwork: consent form, patient identification bands
Drugs - Induction and maintenance agents (e.g. fentanyl, ketamine, rocuronium, sevoflurane)
- Tranexamic acid, calcium chloride, insulin/dextrose, antibiotics
- Emergency drugs
- Blood products checked and loaded into rapid infuser
Patient - Airway equipment including suction and difficult airway equipment
- Venous access: large bore (peripheral, central or both)
- Monitoring: Association of Anaesthetists' standard monitoring, arterial line, temperature probe, syringes and containers for point-of-care blood gas and coagulation measurement
- Urinary catheter
- Nasogastric tube
- Change of sheets or drapes if wet/bloodied to prevent hypothermia
Role allocation - Additional peripheral, and arterial and central venous catheter lines as directed
- Operating the rapid infusion device
- Communicating with blood bank
- Blood runner to transfusion laboratory
- Checking blood products and maintaining tally of usage
- Performing blood gas and viscoelastic haemostatic assay analysis
Induction
In severely unwell patients, surgeons should be scrubbed and ready for immediate knife to skin as even optimal induction may still lead to instability
Blood products should be ready to give via a rapid infusion device facilitating ongoing resuscitation during induction to prevent cardiovascular collapse
A key consideration during induction of anaesthesia is avoiding hypotension and cardiac arrest
sudden increases in arterial pressure are also undesirable, as they may restart bleeding or worsen any intracranial injury
In addition to any ongoing bleeding, hypotension on induction may be secondary to
- loss of sympathetic drive,
- loss of skeletal muscle pump,
- direct myocardial suppression,
- vasodilation
- switch to PPV
- → +ve intrathoracic pressures.
- Exacerbation of any existing PTx or arrhythmia
Major haemorrhage influences the pharmacokinetics of i.v. anaesthetic agents, with animal models showing ↑ plasma drug concentrations with equivalent dosing.
in practice, this means that dose effects may be unpredictable and significant reductions may be necessary to avoid haemodynamic compromise.
Ketamine is the preferred induction agent in trauma because of its relative cardiovascular stability and longer duration of effect
Fentanyl blunts the response to laryngoscopy but also sympathetic drive causing hypotension
Some clinicians advocate for ↑ doses of rocuronium to shorten the prolonged onset times associated with shock.
In the awake, less compromised trauma patient without intracranial injury, a 1:1:1 combination of fentanyl 1 μg/kg, ketamine 1 mg/kg and rocuronium 1 mg/kg is effective. In a shocked patient, this is adjusted to rocuronium 1–2 mg/kg with ketamine 0.5–1 mg/kg, omitting fentanyl. In near- or actual cardiac arrest, further dose reduction or even omission may be appropriate.
Airway in trauma
expecting Difficult airway & need of eFONA
may need MILS
To mitigate haemodynamic effects from the switch to positive pressure ventilation, begin with
- small tidal volumes (200–300 ml),
- low ventilatory frequency (10/min)
- no PEEP.
Over the next few minutes, this can be rapidly increased as tolerated to a lung-protective ventilation (6–8 ml/kg) target, and a frequency suitable for CO2 clearance
Maintenance
Given the altered pharmacology of propofol in haemorrhage, anaesthesia is maintained with a volatile agent such as sevoflurane
Fentanyl, starting in 50μg aliquots and increased as tolerated often to total doses of 15–25 μg/kg, will allow a considerable reduction in MAC of sevoflurane, typically to 0.5
Depth of anaesthesia monitoring may provide reassurance.
may need to repeat TXA & Abx due to haemorrhage
Post-op
intubated to ICU
After surgery, the aim is for resolution of
- shock,
- acidosis,
- hypothermia,
- coagulopathy
- anaemia
achievement of euvolaemia. pH, lactate, and temperature may not return to normal for many hours, but a lack of improvement is a concerning sign
Key points of Critical care management
- vigilance for signs of bleeding requiring re-exploration,
- planning relook surgery if needed,
- replacement of non-sterile invasive resuscitative lines,
- recognition of the consequences of temporising interventions
- for the development of organ failure
?Possibility of applying ERAS elements to non extremis patients
Analgesia
multimodal
IV PCA
paracetamol
NSAIDs
RA (e.g. rectus sheath catheters)
low dose ketamine
References
Anaesthetic management of abdominal trauma - BJA Education
Anaesthetic Management of Abdominal Trauma - BJA Ed
Acute Traumatic Coagulopathy Pathophysiology and Resuscitation - BJA