Anaesthesia, Analgesia and Supportive Care

To select an appropriate sedative or anaesthetic technique for animals with neurological disease, a basic understanding of physiology and pathophysiology of the disease is essential. Discussed in this post are:

  • • The physiological and pathophysiological aspects of neurological disease relevant to anaesthesia and analgesia
  • • The information used to develop a rational approach to anaesthetizing the neurological patient
  • • The supportive care required by animals undergoing anaesthesia and analgesia.

Intracranial pressure

The aim of anaesthesia in animals with central nervous system (CNS) disease is preservation of neuronal function. Normal neuronal function depends on adequate cerebral blood flow.

Factors that influence cerebral blood flow

Cerebral blood flow (CBF) is equal to cerebral pertusion pressure (CPP) divided by cerebral vascular resistance (CVR), where cerebral pertusion pressure is mean arterial blood pressure (MABP) minus intracranial pressure (ICP). Thus:

CBF = (MABP – ICP)/CVR

Regulation of cerebral vascular resistance

Cerebral blood flow is regulated by local mechanisms that alter cerebral vascular resistance, including autoregulation, flow metabolism coupling and chemical regulation.

Autoregulation is a myogenic reflex that maintains constant blood flow by altering vascular resistance in response to changes in transmural pressure. In normal brain tissue, autoregulation operates at CPPs between 50 and 150 mmHg, provided that fluctuations within this range are not rapid. Outside this normal physiological range, cerebral blood flow changes linearly with MABP ().

Flow-metabolism coupling describes the linear relationship between cerebral blood flow and cerebral metabolic rate. Increases in cerebral metabolic rate result in increased consumption of glucose and oxygen and increased production of local tissue metabolites such as H+ ions, adenosine and potassium, which dilate cerebral arterioles and thus increase cerebral blood flow (CBF). Conversely, decreases in cerebral metabolic rate result in decreased cerebral blood flow and cerebral blood volume (CBV), due to arteriolar constriction.

Chemical regulation of cerebral vascular resistance is influenced by many factors. Of relevance to the anaesthetist are the effects of arterial carbon dioxide and oxygen. Carbon dioxide (CO2) is a potent arterial vasodilator in the CNS. Outside the normal physiological range, increases in the partial pressure of arterial CO2 (PaCO2) cause decreased cerebral vascular resistance and increased CBF. Conversely, decreases in PaCO2 promote cerebral vasoconstriction, increased cerebral vascular resistance and associated decreases in cerebral blood flow (). Partial pressure of arterial oxygen (PaO2) also influences CBF: outside the normal physiological range, decreases in PaO2 cause arterial vasodilation and thus increases in cerebral blood flow ().

In normal brain tissue these mechanisms ensure that cerebral blood flow is maintained within adequate levels for normal neuronal function. However, these mechanisms can be altered by disease and by administration of pharmacological agents, with serious consequences.

Factors that influence mean arterial blood pressure

An in-depth discussion of cardiovascular physiology is beyond the scope of this chapter but can be found in Levick (1999).

  • • Systemic arterial blood pressure (SABP) is dependent on cardiac output and systemic vascular resistance (SVR).
  • • Cardiac output is determined by the product of stroke volume (SV) and heart rate (HR).
  • • Stroke volume is influenced by preload, cardiac contractility and afterload.
  • • Preload is influenced by venous return, which is influenced by relative or absolute circulating blood volume.
  • • Afterload is predominantly influenced by vascular tone and peripheral vascular resistance.

Alterations in any of the factors that influence cardiac output or SVR by disease or pharmacological agents can alter MABP and subsequently alter cerebral pertusion pressure and CBF.

Factors that influence intracranial pressure

Increased ICP occurs when pathological increases in intracranial tissue volume exceed compensatory decreases in other intracranial tissues. The result is decreased CPP, which causes neuronal ischae-mia, dysfunction and, ultimately, neuronal death ().

The CNS is surrounded by rigid bony structures. As a result, the volume of the intracranial contents is fixed. Intracranial contents consist of solid tissue, tissue water, cerebrospinal fluid (CSF) and blood. Increases in any of these components must be accompanied by a compensatory decrease in volume of one of the other components to prevent increases in ICP ().

To compensate for increased intracranial volume, CSF and cerebral blood volume are decreased by increased tissue absorption and translocation, and vasoconstriction, respectively. In addition, CSF and venous blood are forced extracranially. Eventually volume compensation is exhausted, with complete compression of venous sinuses and little or no CSF remaining intracranially. Once compensatory mechanisms have been exhausted, small increases in intracranial volume will dramatically increase ICP ().

Factors that contribute to increased intracranial volume and ICP are summarized in Table: Summary of causes and treatment of increased intracranial pressure. Pathological increases in intracranial volume and ICP can be due to increased soft tissue (tumour, abscess, haematoma), increased tissue water (oedema) or increased CSF volume (hydrocephalus). Physiological increases in intracranial volume and ICP are associated with increased cerebral blood volume, which may be venous or arterial.

• Increased cerebral venous blood volume can be due to physiological or pharmacological venodilation or interference with venous flow. Causes of decreased venous flow include: obstruction of jugular veins; ventroflexion of the neck; increased intrathoracic pressure during intermittent positive pressure ventilation (IPPV); and increased central venous pressure (CVP), which could be due to excessive intravenous fluid administration or cardiac failure.

• Increased cerebral arterial blood volume is caused by physiological factors or pharmacological intervention causing arterial vasodilation. Decreases or increases in MABP and associated cerebral pertusion pressure stimulate an autoregulatory response that causes reflex arterial vasodilation or constriction in an attempt to maintain CBF. In contrast, when brain autoregulation is diminished (brain disease, inhalation agents), cerebral blood flow and CBV increase lin’early with MABP. Thus high MABP (hypertension) causes increased cerebral blood flow and associated increases in CBV and ICP, and hypotension results in decreased CBF. Cerebral vasodilation and associated increases in CBF, CBV and ICP are also caused by increased cerebral metabolic rate, increased PaCO2 and decreased PaO2.

Anaesthetic agents alter CBV and ICP by directly affecting the cerebral vasculature or by altering cerebral autoregulation, flow-metabolism coupling and chemical responsiveness.

Table: Summary of causes and treatment of increased intracranial pressure. (ABP = arterial blood pressure; CVP = central venous pressure; IPPV = intermittent positive pressure ventilation)

Mechanism Cause Management
Pathological Mass (tumour, abscess) Mannitol: 0.25-1 .Og/kgi.v.
Tissue fluid (oedema, inflammation) Furosemide 0.7 mg/kg i.v.
Haemorrhage/haematoma Corticosteroids for neoplasia:
Hydrocephalus Methylprednisolone 10-30 mg/kg i.v.
Dexamethasone 0.2-0.5 mg/kg i.v.
Craniectomy and durotomy
Physiological Increased venous blood volume: Decrease venous blood volume:
Jugular vein obstruction Careful patient positioning
Head-down position Head elevation (< 30 degrees)
Increased intrathoracic pressure (as a result of IPPV) Monitor CVP during IPPV and intravenous fluid therapy
Increased CVP; fluid overload
Increased arterial blood volume:
Increased arterial blood volume: Maintain normotension
Increased ABP Ventilate to normocapnia
Increased PaCO2 Supplement oxygen
Decreased PaO2 Decrease cerebral metabolic rate: treat seizures, eliminate pyrexia, choose appropriate drugs
Increased cerebral metabolic rate: seizures, pyrexia, drugs
Pharmacological Direct arterial or venous dilation Select anaesthetic agents that decrease cerebral metabolic rate (thus reducing cerebral blood flow) to counteract effect of vessel dilation
Interference with autoregulation, chemical responsiveness and flow-metabolism coupling
Select agents that minimally alter autoregulation, flow-metabolism coupling and chemical responsiveness

Stabilization of increased ICP

Any patient with increased ICP, regardless of cause, requires stabilization before anaesthesia or sedation for further work-up is considered. Osmotic diuretics such as mannitol are very effective in reducing ICP and are usually the first-line treatment for stabilizing patients with increased ICP. Administration of corticosteroids is found to be beneficial in vasogenic cerebral oedema, such as is associated with neoplasia, but has not been observed to reduce ICP in other disease states. In an emergency, intubation and cautious hyperventilation may be warranted ().

Diuretics

Mannitol is administered at 0.25-1.0 g/kg i.v. over 10-15 minutes. Although an almost immediate effect is seen, peak effect occurs within 60 minutes of administration. Repeated dosing every 4 hours can be used if necessary but ultimately causes dehydration, hypotension and ischaemia.

Mannitol decreases ICP partly by increasing the osmotic gradient between intravascular and extravascular fluid compartments, causing fluid to move out of tissues into the blood. The increase in blood volume decreases ICP due to the dilutional effects on packed cell volume (PCV) and the resultant decrease in blood viscosity. Decreased blood viscosity improves oxygen delivery, which ultimately stimulates cerebral vasoconstriction and decreased cerebral blood volume (). The osmotic effects of mannitol on ICP are effective for 16-48 hours, after which brain tissue accommodates to the newosmolality. Fluid restriction after mannitol therapy has been associated with poor outcome in human patients (), thus it is imperative that intravenous fluid therapy is instigated to ensure that patients remain normovolaemic. Furosemide is a loop diuretic that inhibits the sodium/ potassium/chloride ion pump in the thick ascending loop of Henle, resulting in decreased sodium and water reabsorption. Concurrent administration of furosemide at 0.7 mg/kg i.v. has been reported to be synergistic with mannitol for reducing ICP (). Adverse effects of loop diuretics include hypokalaemia and dehydration; thus fluid and electrolyte balance needs to be monitored closely if these agents are used.

Hyperventilation

Hyperventilation to achieve a PaCO2 of 30 mmHg can be used for stabilization of acute, transient increases in ICP, particularly when herniation is imminent ().

Hyperventilation decreases ICP by causing respiratory alkalosis and stimulates constriction of cerebral arterioles. Prolonged hyperventilation is not recommended, as associated vasoconstriction may worsen neuronal injury by decreasing oxygen supply to normal areas of the brain (). It is therefore recommended that PaCO2 should not decrease below 30 mmHg, thus minimizing ischaemia in normal regions of the brain. The degree of ventilation should be monitored using capnography or, ideally, direct blood gas analysis. It is important to remember that damaged areas of brain lose the ability to autoregulate and do not reliably constrict. When hyperventilation is used to assist with stabilization of the patient with increased ICP, it must be used carefully with close monitoring of the patient.

Haemodynamic stabilization

Adequate cerebral perfusion requires a cerebral pertusion pressure of 50-60 mmHg. In the absence of ICP monitoring, it is recommended that MABP be maintained between 80 and 100 mmHg, in order to ‘achieve’ this cerebral pertusion pressure ().

Cerebral perfusion pressure is determined by the difference between MABP and ICP. Thus, maintenance of cerebral perfusion in patients with increased ICP requires maintenance of adequate MABP. Therapy used to improve MABP, such as intravenousfluid therapy, should be guided by CVP to prevent excessive increases in CVP, which will decrease CSF drainage and exacerbate increases in ICP. Characteristics of fluids that can be used are summarized in Table Summary of crystalloid and colloid fluid characteristics and suitability for use in animals with central nervous system disease (CBV = cerebral blood flow)

Category Type of fluid Osmolality (mOsm/l) Uses Comments
Hypotonic crystalloids 5% glucose 252 Hypoglycaemia: 2 ml/kg/h Blood glucose elevation exacerbates neuronal injury in ischaemic tissues; thus, glucose-containing fluids should be avoided in intracranial and spinal cord disease
Lactated Ringer’s / Hartmann’s solution 250-260 Rehydration: 2 ml/kg/h + % dehydration +losses Intraoperative: 10 ml/kg/h Can increase brain water content, especially if administered in large amounts
Isotoniccrystalloids Polyionic isotonic crystalloid (e.g. Plasmalyte) 312 Rehydration: 2 ml/kg/h + % dehydration + losses Intraoperative: 10 ml/kg/h Preferred rehydration solution for CNS disease
0.9% saline 308 Rehydration: 2 ml/kg/h + % dehydration + losses Intraoperative: 10 ml/kg/h Prolonged use causes hyperchloraemic metabolic acidosis
Isotonic colloids Etherified starch 6% (e.g. Hetastarch) 310 Rapid expansion of blood volume: up to 20 ml/kg/h Maximum dose 20 ml/kg/day to prevent side-effects associated with bleedingSmall dogs/cats (<5 kg) at greater risk of fluid overload
Haemoglobin glutamer-200 (bovine) Not reported Resuscitation (when blood unavailable): up to 10 ml/kg/h Nitric oxide scavenger: may have detrimental effect on cerebral auioregulation and CBF. Use cautiously in neurological patientSmall dogs/cats (<5 kg) at greater risk of fluid overload
Hypertonic crystalloids 7.2% saline 2400 Resuscitation:Dogs: 4-5 ml/kg over 5-10 min

Cats: 2 ml/kg over 5-10 min

Can decrease brain water contentUseful for resuscitation in head traumaMust be used with isotonic crystalloid to prevent tissue dehydration

Colloids and hypertonic saline solutions allow more rapid restoration of circulating blood volume and subsequent normotension, using smaller volumes of fluid than crystalloids. Administration of hypertonic solutions causes plasma volume expansion by osmotic movement of intracellular and interstitial fluid into the intravascular space. This effect may have the added benefit of reducing brain water content and ICP. It is important to remember that cellular and systemic dehydration and electrolyte abnormalities will occur following administration of hypertonic saline unless follow-up administration of isotonic crystalloids or even colloids is performed. Fluid therapy for animals with intracranial disease is discussed in more detail below.

Positioning

Careful positioning of the patient to prevent occlusion of jugular veins and achieve mild head elevation is recommended for animals with increased ICP.

It is important to remember that excessive head elevation will decrease blood pressure within the cerebral cavity, due to the hydrostatic effects of gravity, and thus will decrease CPP. It is recommended that head elevation does not exceed 30 degrees.

Intracranial Disease: Anaesthesia, Analgesia and Supportive Care

Spinal Disease: Anaesthesia, Analgesia and Supportive Care

Special considerations for diagnostic procedures

Myelography

Seizure activity is a well recognized adverse effect of contrast injection. The risk of seizures is influenced by several factors, including: volume and rate of contrast injection; site of injection; size of animal; duration of anaesthesia after injection; and position of animal during injection (). Seizures are more commonly observed after cisternal injection than after lumbar injection. Animals >20 kg in bodyweight are also observed to have a higher incidence of seizures, possibly due to a relatively higher volume of contrast injected ().

To reduce the risk of seizures, dose rate should be calculated from surface area rather than body-weight, the speed of injection should be limited and the head should be elevated as soon as the injection is complete, to allow contrast medium to flow away from the head (). Use of a tilting table allows head elevation while keeping the animal’s spine flat on the table. Pharmacological agents that decrease the seizure threshold should be avoided. ACP, ketamine and medetomidine are reported to decrease seizure threshold () and it is recommended that these agents are not used in animals undergoing myelography. Seizures have been reported to occur up to 6 hours after injection of contrast medium, and thus animals should be closely monitored during this time. If seizures occur, administration of diazepam (0.2-0.5 mg/kg i.v.) is recommended.

Cardiopulmonary side-effects have also been observed during or immediately after injection of contrast medium, including apnoea, tachypnoea, bradycardia, tachycardia, arrhythmias, hypotension and hypertension (). Some of these effects are associated with discomfort or pain of injection and can be minimized by slow injection of contrast and ensuring adequate depth of anaesthesia during injection. To detect these problems, careful monitoring of cardiopulmonaryfunction is necessary during myelography.

Magnetic resonance imaging

The main considerations for anaesthetizing patients with spinal and intracranial disease are described above. In addition there are several important considerations unique to anaesthetizing a patient within a magnetic field ().

Ferromagnetic objects can become projectile and may result in injury to the patient or personnel within the scanning room. It is essential that these objects remain outside the 50 gauss line ().

Non-ferromagnetic objects and implants have the potential to distort or degrade the quality of the image. Anaesthetic machines are required to be as close to the patient as possible to minimize the length of anaesthetic circuits, and should be composed of non-ferromagnetic materials.

Non-ferromagnetic objects within a magnetic field (e.g. ECG leads) have the potential to induce electric currents, leading to heating and burns. The risk of burns can be minimized by insulating the wires, separating the wires from skin by padding, avoiding large loops of wire that allow induction of currents, and applying sensors as far away as possible from the imaged area.

Monitoring the anaesthetized patient during MRI has inherent limitations. Equipment used for monitoring must be MRI-safe and ideally MRI-compatible. MRI-compatible equipment has been shown to be safe, not to significantly reduce the diagnostic quality of the image and not to have its operation affected by the scanning procedure. At present, MRI-compatible equipment is available that allows distant monitoring of animals during the procedure. Where cost is limited, some monitoring equipment such as capnography and oscillometric methods of blood pressure measurement can be used if the electrical components are beyond the 50 gauss line.

Cerebrospinal fluid collection

Collection of CSF may be performed by cistemal or lumbar puncture (). Cistemal puncture requires neck flexion; this can kink the endotracheal tube, causing respiratory obstruction, and also obstruct the jugular veins, impairing venous drainage and contributing to increased ICP. Positive pressure ventilation is essential during cistemal puncture to ensure adequate ventilation and normocapnia.

Endotracheal tubes reinforced with coiled wire resist kinking and can be used to prevent airway obstruction when the neck is flexed for collection of CSF. However, as these tubes contain metal, they are not suitable for use in animals undergoing concurrent MRI.

In animals with increased ICP, collection of CSF carries the risk of herniation. When sampling is essential for diagnosis and treatment of the animal, reducing arterial CO2 to 30 mmHg by hyperventilation during the sampling period may reduce the risk of cerebral herniation.

Neuromuscular Disease: Anaesthesia, Analgesia and Supportive Care

Anthea L. Raisis and Jacqueline C. Brearley

 

Selections from the book: “BSAVA Manual of Canine and Feline Neurology”, 2004