Introduction

The patient in critical condition offers a great challenge for the anesthetists, who must use all their knowledge and skills to try to stabilize the patient's condition before it is subjected to medical or surgical maneuvers designed to treat the pathology.

Anesthetic Protocols in Critically Ill Patients

Due to the wide range of entities found in critically ill patients and the different impact each one has on the body homeostasis, it is essential to evaluate each one separately, set goals and implement the monitoring level necessary to perform a safe anesthetic procedure.

This work reviews, succinctly, some common critical situations frequently encountered in critically ill patients and how to approach the anesthetic management.

Special Features of the Anesthetic Protocol in Patients with Different Pathologies

Hypovolemic Patients

 Therapeutic goals

 Reset cardiac output

 To maintain an adequate venous return

 Ensure tissue perfusion pressure

 Maintain a ΔT < 6°C

 Ensure an adequate level of analgesia during the recovery period

 Causes of hypovolemia

 Hemorrhage

 Hypoalbuminemia

 Dehydration

 Poor distribution of blood volume available

 For example, as a result of the administration of vasodilator anesthetics (relative hypovolemia)

 In order to make a good categorization of the patient, indicators of preload and antegrade flow parameters such as capillary refill time, color of mucous membranes, blood pressure and cardiac output should be monitored.

 Hypovolemic patients often experience episodes of hypotension during anesthetic induction.

 It is recommended to ensure adequate volemic resuscitation by administering fluids before induction.

 Concomitant use of vasopressors before the induction should be considered.

 Anesthetic drugs recommended in the hypovolemic patient.

 Drug doses should be decreased during induction.

 In all cases, the administration of inductors must be slow and titrate.

 Both ketamine (except in cases of catecholamine depletion) and etomidate preserve cardiovascular function.

 We recommend the adjunctive administration of opioids or benzodiazepines during the induction of critical patients.

 In these patients, the use of propofol or thiopental sodium may worsen hypotension.

Abdominal Trauma

 Therapeutic goals

 Reduce abdominal pressure (IAP < 10 mm Hg)

 Establish an adequate venous return (CVP 3–8 mm Hg)

 Ensure tissue perfusion (MBP > 65 mm Hg)

 Replace the volemia (ΔPp < 13%)

 Maintain urine output (> 0.5 ml/kg/hr)

 Maintain a ΔT < 6°C

 Ensure an adequate level of analgesia during the recovery period

 The most affected organs in the abdominal trauma are:

 Intestine

 Liver

 Spleen

 Pancreas

 Major blood vessels

 The findings of higher prevalence in patients with abdominal trauma are:

 Hemoabdomen (rupture of liver, spleen, and large abdominal vessels)

 Abdominal hernias

 Rupture of ureters and/or bladder

 The trauma is usually associated with a significant increase in intra-abdominal pressure (IAP), which in turn promotes:

 Decrease in venous return and cardiac output.

 Compression on the diaphragm and collapse of the lung parenchyma.

 Impairment of splanchnic perfusion proportionally to the increase in IAP.

 Reduction of renal perfusion related to the decrease of urine output.

 Avoid, if possible, anesthetizing hypovolemic patients.

 In hypovolemic patients, make resuscitation based on fluids.

 Administration of large boluses of fluid should include:

 Crystalloid (isotonic solutions and/ or hypertonic, depending on the current patient osmolality)

 Colloids

 The use of fresh blood or derivatives may be vital in the management of bleeding that affects the packed cell volume.

 It is suggested to avoid anesthesia and to transfuse patients with hemoglobin values below 5–7 g/dl.

 During anesthesia maintain hemoglobin ≥ 8 g/dl.

 To categorize the patient, the evolution of metabolic markers of perfusion and tissue oxygenation should be analyzed.

 In patients with severe acute anemia it could be found:

 Decrease of the O₂ partial pressure in mixed venous blood (PvO₂)

 Increased arteriovenous O₂ gradient (suggesting a high tissue extraction of O₂)

 Increased arteriovenous PaCO₂ gradient

 Elevated lactate (late indicator of tissue perfusion deficit)

 A common finding in abdominal trauma is the uroperitoneum that occurs as a consequence of damage to the urinary tract (kidney, ureter, bladder, abdominal urethra).

 It is important, as far as possible, to restore electrolyte balance before anesthetizing the patient.

 Among the changes, the most frequent is the hyperkalemia.

 It is considered hyperkalemia when plasma values are above 5.5 mEq/L.

 Values of 7.5 mEq/L may compromise the patient's life (bradycardia, atrial fibrillation, sinus rhythm, ventricular fibrillation, or ventricular asystole).

 Strategies to reduce hyperkalemia:

 Administration of calcium gluconate 10% (0.5–1.5 mL/kg IV) slowly to reduce the occurrence of cardiac arrhythmias).

 Coadministration of dextrose (0.7 to 1 g/kg IV) and regular insulin (0.1 to 0.5 IU/kg IV).

 Reduces serum K+.

 Administration of sodium bicarbonate (1 to 2 mEq/kg IV) slowly (10 to 15 minutes).

 Extracellular potassium migrates into the intracellular space.

 All these maneuvers are aimed to correct the disequilibrium and temporarily stabilize the patient. However, the surgery will be necessary to ensure a favorable outcome.

 Anesthetic protocol in patients with abdominal trauma

 In hypovolemic patients comply with the rules patterned in the previous item.

 In case of having to compensate a patient with active bleeding maintain a tolerant attitude on the hypotension (permissive hypotension).

 Whenever possible, administer pain medication to reduce the sympathetic response.

 Until having a definitive diagnosis the incorporation of drugs affecting gastrointestinal motility or abdominal organ function should be avoided.

 The administration of morphine has a high incidence of vomiting and gastrointestinal stasis.

 Lidocaine significantly increases the motility of the gastrointestinal tract (indirectly by blocking inhibitory signals and reducing the formation of inflammatory substances and free radicals) and provides analgesia.

 Meperidine has antispasmodic effects (but promotes histamine release).

 Antiinflammatory drugs (NSAIDs) can precipitate an acute kidney injury in hypovolemic/hypotensive patients.

 NSAIDs or COX-1 inhibitors can promote bleeding through its antiplatelet effect.

 Dipyrone (Metamizol) (25 mg/kg) is excellent for visceral analgesia.

 Ketamine is primarily eliminated by glomerular filtration rate in cats.

 Considered in oliguric patients with urinary tract injury.

 Ketamine is eliminated primarily by hepatic metabolism in dogs.

 Considered in patients with reduced hepatic plasma flow (increased IAP, decreased MBP).

 The removal rate for propofol tends to remain stable in patients with liver failure and/or kidney failure, partly due to extrahepatic metabolism.

 However, it may promote hypotension.

 When the lung parenchyma is healthy inhalation anesthesia is adequate.

 The use of locoregional blocking techniques (TAP block) is an alternative in patients with ruptured abdominal wall.

Cerebral Contusion

 Therapeutic goals

 Reduce the high intracranial pressure (ICP).

 Maintain adequate cerebral perfusion pressure (CPP).

 Moderate hypothermia may be beneficial.

 Ensure an adequate level of analgesia during the recovery period.

 The impact of trauma on the cranial vault may produce contusion or laceration of the cerebral cortex.

 Brain parenchymal damage can also occur as a result of acceleration-deceleration phenomenon.

 The skull vault is noncompliant, consisting mainly of 3 tissues: the brain, blood and cerebrospinal fluid.

 ICP increases as a result of an increase in any component of the cavity.

 The ICP increase aggravates parenchymal ischemia in the brain and accelerates cell damage.

 The determinant of cerebral tissue perfusion is known as PPC.

 The PPC is determined by the difference between mean arterial pressure (MAP) and ICP.

 Decreases in MAP or increased ICP invariably produce a decrease in the PPC, and therefore cerebral ischemia will be present.

 In patients with brain trauma, the ability to self-regulate the blood flow in the presence of metabolic changes in O₂ consumption or changes in PaO₂ and PaCO₂ is altered.

 As in veterinary medicine we rarely determine the intracranial pressure (ICP), the approach to follow is:

 In patients with head injury in which there is a suspicion of increased ICP, MBP should remain above 60 mm Hg.

 Where there is suspicion of raised ICP (abnormal behaviors, changes in pupillary diameter [anisocoria], seizures, bradycardia from extra cardiovascular source), it is recommended to keep the MBP above 90 mm Hg to preserve maximum cerebral flow.

 Drug of choice in patients with head injury

 Propofol and thiopental are inducers of choice in patients with cranial trauma due to their protective effect on the cerebral hemodynamic profile.

 Propofol is the drug of choice for the maintenance of these patients.

 The association of propofol with opioids, benzodiazepines and/or local anesthetics such as lidocaine, can lower doses during induction and maintenance.

 Inhalation anesthetics decrease brain metabolism but can increase blood flow resulting from vasodilation.

 In all cases, the cough reflex must be avoided.

 Endotracheal intubation should be preceded by topical application of lidocaine 1% on the entrance of the larynx 20 seconds before the intubation.

 If inhalation anesthetics are used, associate them with other drugs to keep MAC values < 1, to preserve autoregulation of blood flow and cerebral flow-metabolism relationship.

 Ketamine is excluded from the protocol due to its cerebral vasodilator effect.

Pulmonary Contusion

 Therapeutic goals

 To ensure oxygenation

 To keep the cardiac output constant

 To reduce the oxygen consumption of skeletal muscle

 To ensure tissue perfusion

 To moderate the hypothermia

 To reduce the dose of general anesthetics

 To ensure an adequate level of analgesia during the recovery period

 Pulmonary contusion is a common finding in patients exposed to chest trauma.

 The pulmonary contusion generates hemorrhage areas that drain blood into the lumen of the alveolus.

 Accumulation of blood causes atelectasis and collapse of small airways, promoting hypoxemia as a result of impaired ventilation/perfusion.

 Signs of respiratory distress are present as well as its immediate consequences: hypoxemia and hypercapnia.

 Supportive therapy usually includes administration of oxygen and ventilatory support (positive pressure mechanical ventilation).

 Protective ventilation scheme:

 VT: 6 to 8 ml/kg

 PEEP: 8 ± 2 cm H₂O (ideal titrate PEEP)

 FiO₂: ≤ 0.5 (in cases of severe hypoxemia FiO₂ should be: 1 vol%)

 In cases of massive pulmonary hemorrhage, use of monobronchial intubation is often helpful.

 In patients with severe hypoxemia, implementation of an adequate level of PEEP is often needed to ensure acceptable levels of oxygenation (PaO₂ at least 60 mm Hg).

 To define the magnitude of the problem is highly advisable to monitor arterial blood gases (PaO₂, PaCO₂, PaO₂/FiO₂).

 In patients with pulmonary contusion, the use of inhalational anesthetic induction drugs should be avoided because the partial pressure of these compounds depends entirely on the alveolar-capillary diffusion.

 To provide analgesia and sedation, opioids can be used at low doses.

 The induction can be performed with propofol, thiopental, etomidate or ketamine, depending on the patient's physical condition (ASA).

 For maintaining anesthesia in patients with pulmonary contusions, propofol (10–30 mg/kg/hour) is highly recommended.

 The use of loco-regional analgesia helps to strengthen and helps reduce the dose of general anesthetics.

 For surgical approach of the thoracic cavity blocking thoracic paravertebral root is the procedure of choice.

 The use of neuromuscular relaxants (atracurium 0.2 mg/kg, vecuronium 50 mg/kg, rocuronium 0.6 mg/kg) inhibits the activity of skeletal muscle, decreasing the work of breathing (WOB) and increasing the efficiency of oxygen intake of vital organs (brain, myocardium, and splanchnic area).