Friday, December 31, 2010
PULMONARY ARTERIAL HYPERTENSION
Primary pulmonary hypertension (PAH) is a rare disease with an incidence of one to two cases per million people in the general population. While the majority of cases of pulmonary hypertension not associated with other medical conditions are sporadic, familial autosomal dominant inheritance accounts for 10% of these cases. The median period of survival after a diagnosis of idiopathic PAH is 2.8 years, with most patients succumbing to progressive right ventricular (RV) failure. Patients with idiopathic PAH are at risk of perioperative RV failure, hypoxemia, and coronary ischemia. Their risk may be as high as 28% for respiratory failure, 12% for cardiac dysrhythmias, 11% for congestive heart failure, and 7% for overall perioperative mortality for noncardiac surgery.
The pulmonary arteries normally have a systolic pressure of 18 to 25 mm Hg, a diastolic pressure of 6 to 10 mm Hg, and a mean pressure of 12 to 16 mm Hg. Pulmonary arterial hypertension is defined as a mean pulmonary artery pressure higher than 25 mm Hg at rest or higher than 30 mm Hg with exercise. Idiopathic PAH, previously called primary pulmonary hypertension, is that which occurs in the absence of left-sided heart disease, myocardial disease, congenital heart disease, and any clinically significant respiratory, connective tissue, or chronic thromboembolic disease. With idiopathic PAH, pulmonary artery occlusion pressure is no more than 15 mm Hg, and pulmonary vascular resistance (PVR) is higher than 3 Wood units (mm Hg/L/min) ( Table 5-9 ).
PVR is expressed in dynes/sec/cm-5, with normal PVR = 50–150 dynes/sec/cm-5
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PVR is expressed in Wood units (mm Hg/L/min), with normal PVR = 1 Wood unit
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PAH often presents with vague symptoms including breathlessness, weakness, fatigue, and abdominal distention. Syncope and angina pectoris are indicative of severe limitations of cardiac output and possible myocardial ischemia.
On physical examination, the patient may exhibit a parasternal lift, murmurs of pulmonic insufficiency (Graham-Steell murmur) and/or tricuspid regurgitation, a pronounced pulmonic component of S2, an S3 gallop, jugular venous distention, peripheral edema, hepatomegaly, and ascites.
The laboratory evaluation and diagnostic studies used in the workup of pulmonary hypertension of any cause are listed in Table 5-11 . A 6-minute walk test can be administered to assess functional status and noninvasively follow the progress of therapy. Right heart catheterization provides a definitive means to determine disease severity and to ascertain which patients can respond to vasodilator therapy. A potent vasodilator such as prostacyclin, NO, adenosine, or prostaglandin E1 is administered. The vasodilator test is considered positive, i.e., the patient is a responder, if PVR and mean pulmonary arterial pressure both decrease acutely by 20% or more. Only about one fourth of patients will have a favorable response to the vasodilator test.
Diagnostic Modality
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Key Findings
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Chest radiograph
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Electrocardiography
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Two-dimensional echocardiography
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Pulmonary function tests
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V/Q scan
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Pulmonary angiography
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Chest CT scan
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Abdominal ultrasound or CT scan
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Blood tests
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Sleep study
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The normal pulmonary circulation can accommodate flow rates ranging from 6 to 25 L/min with minimal changes in pulmonary artery pressure. As a result of pulmonary vasoconstriction, vascular wall remodeling and thrombosis in situ, PAH develops. RV wall stress increases in response to the increase in afterload produced by pulmonary hypertension. Both RV stroke volume and the volume available for left ventricular filling are reduced, leading to low cardiac output and systemic hypotension. RV dilation in response to the increased wall stress results in annular dilation of right-sided heart valves producing tricuspid regurgitation and/or pulmonic insufficiency. The right ventricle receives coronary blood flow during both systole and diastole. RV myocardial perfusion can be dramatically limited as RV wall stress increases and RV systolic pressure approaches systemic systolic pressure.
Patients with PAH are at risk of hypoxemia by three mechanisms: (1) as right-sided pressures increase, right-to-left shunting can occur through a patent foramen ovale; (2) in the presence of a relatively fixed cardiac output, the increased oxygen extraction associated with exertion will produce hypoxemia; and (3) V/Q mismatch can result in perfusion of poorly ventilated alveoli. If hypoxic pulmonary vasoconstriction occurs, overall pulmonary hypertension will be worsened.
Oxygen therapy can be helpful in reducing the magnitude of hypoxic pulmonary vasoconstriction. It has been studied primarily in patients with chronic obstructive pulmonary disease, and in this situation, it clearly improves survival and reduces progression of pulmonary hypertension. Anticoagulation may be recommended because of the increased risk of thrombosis and thromboembolism due to sluggish pulmonary blood flow, dilation of the right heart, venous stasis, and the limitation in physical activity imposed by this disease. Diuretics can be used to decrease preload in patients with right heart failure, especially when hepatic congestion, ascites, and severe peripheral edema are present.
The first class of drugs to provide dramatic long-term benefit in patients with PAH was calcium channel blockers. Calcium channel blockers are administered to patients who exhibit a positive response to a vasodilator trial in the cardiac catheterization laboratory. Nifedipine, diltiazem, and amlodipine are the most commonly used calcium channel blockers for this purpose and have been shown to improve 5-year survival.
Phosphodiesterase inhibitors produce pulmonary vasodilation and improve cardiac output. Sildenafil (Viagra) administration has been associated with improved exercise capacity and reduction in RV mass, although long-term mortality benefits have not yet been proven. Phosphodiesterase inhibitors inhibit the hydrolysis of cyclic guanosine monophosphate, reducing intracellular calcium concentration and effecting smooth muscle relaxation. They are effective when given alone and can augment the efficacy of inhaled NO.
Inhaled NO in concentrations of 20 to 40 ppm can be used to treat PAH. When inhaled, NO diffuses into vascular smooth muscle where it activates guanylate cyclase, increasing intracellular cyclic guanosine monophosphate, which reduces intracellular calcium concentration, resulting in smooth muscle relaxation. After diffusing into the intravascular space, NO binds to hemoglobin, forming nitrosylmethemoglobin, which is rapidly metabolized to methemoglobin and excreted by the kidneys. All NO is rendered inactive in the pulmonary circulation, thereby minimizing systemic effects. Because it is administered via inhalation, NO is preferentially distributed to well-ventilated alveoli, causing vasodilation in these areas. This improves ventilation/perfusion matching and improves oxygenation. NO has been shown to improve oxygenation and lower pulmonary arterial pressure in acute respiratory distress syndrome and in other conditions associated with severe pulmonary hypertension, but it has not been shown to reduce mortality in these situations. Problems associated with NO administration include rebound pulmonary hypertension, platelet inhibition, methemoglobinemia, formation of toxic nitrate metabolites, and the technical requirements for its application.
Prostacyclins are systemic and pulmonary vasodilators that also have antiplatelet activity. The prostacyclins reduce PVR and improve cardiac output and exercise tolerance. However, complications such as worsened intrapulmonary shunting, rebound pulmonary hypertension, and problems associated with the route of administration, such as systemic hypotension, infection, and bronchospasm, can occur. Prostacyclins can be administered by continuous infusion in the short term and the long term (by a pump attached to a permanent indwelling central venous catheter), by inhalation, and by intermittent subcutaneous injection. All prostacyclins demonstrate significant improvements in cardiopulmonary hemodynamics, at least in the short term, but have not yet provided evidence of sustained improvement or a decrease in mortality. Currently used prostacyclins include epoprostenol (Flolan), treprostinil (Remodulin), and iloprost (Ventalis).
Endothelin interacts with two receptors: endothelin A and endothelin B. The endothelin A receptors cause pulmonary vasoconstriction and smooth muscle proliferation, whereas the endothelin B receptors produce vasodilation via enhanced endothelin clearance and increased production of NO and prostacyclin. Endothelin receptor antagonists have been shown to lower PA pressure and PVR and to improve RV function, exercise tolerance, quality of life, and mortality. The only endothelin receptor antagonist currently available for general use in the United States is bosentan (Tracleer).
RV assist devices can be used in severe pulmonary hypertension and right heart failure. Balloon atrial septostomy is an investigational procedure that creates an atrial septal defect and allows right-to-left shunting of blood to decompress the right heart. At the expense of an expected and generally well-tolerated decrease in arterial oxygen saturation, it has been shown to improve exercise tolerance. Currently, this procedure is reserved for treatment of terminal right heart failure and as a bridge to cardiac transplantation. The benefits of extracorporeal membrane oxygenation are well established in children, but this modality has not found widespread use in the adult population. Lung transplantation is the only curative therapy for many types of PAH. Long-term survival is similar with single or bilateral lung transplantation.
The risk of right heart failure is significantly increased in patients with PAH during the perioperative period. Mechanisms for this include increased RV afterload, hypoxemia, hypotension, and inadequate RV preload. Medications for PAH should be continued throughout the perioperative period. Continuous infusions of pulmonary vasodilators should be maintained at their usual doses to prevent rebound pulmonary hypertension. Diuretics may be needed to control edema, but excessive diuresis may dangerously reduce RV preload. Reduction in systemic vascular resistance by inhalational anesthetics or sedatives may be dangerous because of the relatively fixed cardiac output. Hypoxia, hypercarbia, and acidosis must be aggressively controlled because these conditions increase PVR. Maintenance of sinus rhythm is crucial. The atrial “kick” is necessary for adequate right and left ventricular filling.
In a patient with newly diagnosed PAH who is not yet on long-term therapy, administration of sildenafil or L-arginine preoperatively may be helpful. Patients on long-term pulmonary vasodilator therapy must have that therapy continued. Systems for inhalation of NO or prostacyclin should be immediately available. Sedatives should be used with caution because respiratory acidosis may increase PVR. Opioids, propofol, thiopental, and depolarizing or nondepolarizing neuromuscular blockers may all be used safely. Ketamine and etomidate may suppress some mechanisms of pulmonary vasorelaxation and should be avoided. Epidural anesthesia has been used for cesarean delivery and other suitable surgical procedures, but close attention must be paid to intravascular volume and systemic vascular resistance. It is also important to remember that prostacyclins and NO can inhibit platelet function. The level of regional anesthesia should be induced slowly and with invasive hemodynamic monitoring so that adjustment in cardiac variables can be made promptly.
Central venous catheterization is recommended, although care must be taken in the placement of central venous and pulmonary artery catheters because disruption of sinus rhythm by the catheter or wire can be a critical event. Intra-arterial blood pressure monitoring is recommended.
Inhalational anesthetics, neuromuscular blockers and opioids, except those associated with histamine release, can be used for maintenance of anesthesia. Hypotension can be corrected with norepinephrine, phenylephrine, or fluids. A potent pulmonary vasodilator such as milrinone, nitroglycerin, NO, or prostacyclin should be available to treat severe pulmonary hypertension should it develop. During mechanical ventilation, fluid balance and ventilator adjustments must be set to prevent a decrease in venous return.
Patients with PAH are at risk of sudden death in the early postoperative period due to worsening PAH, pulmonary thromboembolism, dysrhythmias, and fluid shifts. These patients must be monitored intensively in the postoperative period to help maintain hemodynamic variables and oxygenation at acceptable levels. Optimal pain control is an essential component of the postoperative care of these patients.
Forceps delivery to decrease patient effort is recommended. Nitroglycerin should be immediately available at the time of uterine involution because the return of uterine blood to the central circulation may be poorly tolerated in the parturient with PAH.
ANAESTHESIA FOR THE PATIENT WITH
PULMONARY HYPERTENSION
ANAESTHESIA TUTORIAL OF THE WEEK 228
JUNE 2011
Dr Sarah Thomas, Senior Anaesthetic Registrar
Royal Hobart Hospital
Correspondence to sarah.thomas@dhhs.tas.gov.au
QUESTIONS
Before continuing, consider the following scenario and question. The answers can be found at the end
of the article, together with an explanation.
You are to anaesthetise a 65-year-old woman for laparoscopic sigmoid colectomy. She has recently
been diagnosed with colorectal carcinoma. The patient has been a heavy smoker in the past and has
severe chronic obstructive pulmonary disease (COPD), with secondary pulmonary hypertension. She
also has essential hypertension. Medications include a beta-blocker, ACE inhibitor, inhaled
steroid/beta-agonist and aspirin.
What are your concerns in anaesthetising this patient?
INTRODUCTION
The disease spectrum of Pulmonary Hypertension (PH) has received greater interest in the past decade,
as specific therapies have been developed and survival has improved. More patients with PH are now
presenting for surgery, and this poses a challenge to the anaesthetist. Knowledge of the underlying
physiology is paramount in preventing the feared complication of right heart failure.
DEFINITION AND CLASSIFICATION
Pulmonary Hypertension is defined as a mean pulmonary artery pressure (PAP) >25mmHg at rest with
a pulmonary capillary wedge pressure <12mmHg. Pulmonary hypertension is considered moderately
severe when mean PAP >35mmHg. Right ventricular failure is unusual unless mean PAP is
>50mmHg.
The World Health Organisation classifies pulmonary hypertension by aetiology into five groups. The
disease, including its classification, was comprehensively reviewed at the 4
th World Symposium on
Pulmonary Hypertension in 2008.
Table 1: Clinical classification of pulmonary hypertension
1 Pulmonary Hypertension (PAH)
2 Pulmonary hypertension owing to left heart disease
3 Pulmonary Hypertension owing to lung disease
4 Chronic thromboembolic pulmonary hypertension (CTEPH)
5 Pulmonary hypertension with unclear multifactorial mechanisms
Group 1 includes the disease idiopathic pulmonary hypertension (formerly known as primary
pulmonary hypertension), as well as PH associated with connective tissue disorders. This group of
diseases share similar pathological findings and clinical appearance. The incidence of idiopathic PH is
higher than previously thought, although remains relatively rare at 15 per million.
Of greater interest to the anaesthetist are the more common forms of PH: those due to left heart disease
(group 2) and those due to lung disease (group 3). Cardiac anaesthetists have long been familiar with
PH due to left heart disease, which often occurs in patients undergoing cardiac surgery. Examples
would include patients with mitral valve disease undergoing valve replacement, or patients with severe
LV failure undergoing coronary bypass surgery.
Non-cardiac anaesthetists are more likely to encounter PH in patients with lung disease. Underlying
diseases include COAD, interstitial lung disease, and sleep disordered breathing. The majority of
patients in this group have modest PH.
PITFALLS IN DIAGNOSIS
Pulmonary hypertension may be suspected after patient assessment based on history, examination,
ECG and chest x-ray. The symptoms of PH are non-specific, and diagnosis can be delayed.
If PH is suspected, transoesophageal echocardiography (TTE) is usually the first investigation
undertaken. TTE utilizes Doppler across a tricuspid regurgitant jet, to estimate pulmonary artery
pressure. This technique has been shown to under or over estimate PAP in up to half of patients at risk
of PH, and therefore as a diagnostic test has limitations in accuracy.
Right heart catheterization is required to confirm the diagnosis. A vasodilator challenge forms part of
this assessment.
UNDERSTANDING THE PHYSIOLOGY
Providing anaesthesia to patients with PH poses some challenges. An underlying knowledge
of the cardiovascular pathophysiology is paramount to providing safe anaesthesia in these
patients.
Right ventricular output is dependent on preload, afterload, contractility and heart rate.
Consideration must be given to optimizing each of these parameters.
Raised pulmonary vascular resistance (PVR) places an additional pressure load on the right
ventricle. The right heart is poorly designed to deal with these increases in afterload. A rise
in PVR and hence right ventricular afterload can put the right heart into failure. Left
ventricular failure can then ensue, due to both reduced volume reaching the left heart, and
septal interdependence.
Factors which can raise PVR include hypoxia, hypercarbia, hypothermia, acidaemia, and
pain. Anaesthetic technique is aimed at preventing these occurrences.
The coronary circulation to the right heart is dependent on perfusion pressure at the aortic
root, which in turn is dependent on cardiac output and systemic vascular resistance (SVR).
SVR must be aggressively defended in order to maintain coronary perfusion to the right heart.
Ischaemia to the right ventricle can put in place a downward spiral of right heart failure, with
ensuing cardiovascular collapse.
ANAESTHETIC TECHNIQUES
Many anaesthetic techniques have been employed in anaesthetising patients with pulmonary
hypertension. The actual technique chosen is probably less important than the manner in
which it is executed.
Extended monitoring will be useful. Invasive blood pressure monitoring is ideal as it will aid
early and aggressive treatment of systemic hypotension. A pulmonary artery catheter can be
useful in monitoring trends in PAP. A rising PAP may indicate a rising PVR or a failing right
ventricle (RV). Transoesophageal echocardiography or other cardiac output monitors can
also be useful.
An effort to obtund the response to laryngoscopy should be made.
A variety of anaesthetic induction drugs have been safely employed in patients with PH. One
technique would be to use a combination of midazolam and fentanyl. Etomidate has been
described as an ideal agent in PH. Propofol and thiopentone have also been used without
problems. Concern has been raised that ketamine may raise PVR, however it too has been
utilized safely in humans with PH.
Non-depolarising and depolarising muscle relaxants can be used safely, and should be
chosen based on airway management issues.
A balanced anaesthetic of volatile agent and opioids can be used as maintenance. All of the
commonly used modern volatile agents have been safely used in PH, and there is no
evidence to recommend one over the other. Nitrous oxide should be used with caution as it
may raise PVR.
A systemic vasoconstrictor such as phenylephrine, noradrenaline or metaraminol should be
on hand to treat reductions in systemic blood pressure. A carefully titrated infusion may be
commenced at induction.
Inotropes can be employed to improve right heart contractility but they are often more
beneficial to the left heart than the right heart. The inodilators such as milrinone and
dobutamine will cause systemic vasodilation and hence reduce coronary perfusion pressure,
which limits their utility.
RV failure and raised PVR can be targeted with inhaled selective pulmonary vasodilators.
Agents such as nitric oxide and prostacyclin are increasingly being employed perioperatively
in these patients.
Neuraxial anaesthesia and analgesia, can be used safely in PH, however the anaesthetist
must be vigilant about the cardiovascular consequences of sympathetic blockade. There are
no alpha-1 adrenoreceptors in the pulmonary circulation, hence it is unlikely that neuraxial
blockade has a direct effect on PVR. Systemic vasodilation however, will reduce aortic
coronary perfusion pressure, as well as venous return to the right heart. A decrease in right
atrial filling can reduce stretch on atrial receptors, resulting in reflex bradycardia. Loss of the
cardio-accelerator fibres at T1-T4 may result in bradycardia and loss of inotropy. Bradycardia
and hypotension can cause right heart failure and can be lethal in patients with PH.
SUMMARY OF ANAESTHETIC TECHNIQUES IN PH
Avoid any stimulus which can increase PVR including: nitrous oxide, adrenaline, dopamine,
protamine, serotonin, thromboxane A2, prostaglandins such as PGF2alpha and PGE2,
hypoxia, hypercarbia, acidosis, PEEP and lung hyperinflation, cold, anxiety and stress.
If PVR is increased it can be reduced by: hypocarbia (via hyperventilation), nitric oxide,
morphine, glyceryl trinitrate, sodium nitroprusside, tolazoline, prostacycline (PGI2),
isoprenaline, and aminophylline.
Aims are to avoid marked decreases in venous return (correct blood and fluid loss quickly),
avoid marked decreases in SVR, avoid drugs which cause myocardial depression, and to
maintain a normal heart rate
A feared complication of pulmonary hypertension is right
heart failure
Understanding the physiology of right ventricular function
and coronary perfusion are important when anaesthetising
patients with pulmonary hypertension
Anaesthetic aims in PH are to avoid increased PVR, to
avoid marked decreases in venous return or SVR, to avoid
myocardial depression and to maintain normal heart rate.
SUMMARY
ANSWERS TO QUESTIONS
Your concerns in anaesthetising this patient may include:
1. The presence of severe systemic disease in a patient undergoing intermediate risk surgery.
Optimisation of the patient’s chronic obstructive pulmonary disease and pulmonary
hypertension is warranted pre-operatively.
2. The cardiovascular and respiratory sequelae of pneumoperitoneum, trendelenburg position,
and potentially prolonged surgery.
3. Anticipation and prevention of perioperative right heart failure in the patient with pulmonary
hypertension.
4. Provision of excellent perioperative pain relief, especially in the patients with lung disease, to
reduce the risk of respiratory complications.
REFERENCES and FURTHER READING
Pritts CD and Pearl RG. Anaesthesia for patients with pulmonary hypertension. Current Opinion in
Anaesthesiology 2010, 23:411-416
Mehta S and Little S. Editorial: Screening for Pulmonary Hypertension in Scleroderma. Journal of
Rheumatology 2006; 33:2 204-206
Manecke GR. Anaesthesia for pulmonary endarterectomy. Semin cardiovasc thorac surgery 18: 236-
242
Slinger PD. Anaesthetic planning for the patient with co-existent disease: the patient with lung disease.
New York Society of Anesthesiologists, 64
th
Annual PGA. Scientific Panel December 2010
Thursday, December 30, 2010
Anesthesia for ophthalmic surgery
Anesthesia for ophthalmic surgery
Intraocular pressure dynamics
Factors affecting IOP:
Effect of anesthetic drugs on IOP
Inhalational anesthetics decrease IOP in proportion to the depth of anesthesia due to multiple causes:
Topically administered antichlonirgic drugs result in papillary dilataion whichmay precipitate angle closure glaucoma. Premedication with systemically administered atropine is not associated with intraocular hypertension. Glucopyrrolate may provide a greater margin of safety by preventing its passage into the central nervous system.
Systemic effects of ophthalmic drugs
The occulocardic reflex
Open-Eye Surgical Procedures.
Premedication
Intraocular pressure dynamics
The eye can be considered a hollow sphere with a rigid wall with intraocular pressureof 10-20 mmhg
Factors affecting IOP:
- Volume of the content of the globe: obstruction to aqueous humor outflow increase IOP as in case of glucouma
- External pressure on the eye due to decreasing the size of the globe without proportional change in the volume of its content e.g
pressure on theeye
from tightly fitted mask
- Improper prone position
- Retrobulbar hge
- Cardiac and respiratory variables:
1-Central venous pressure:
A rise in venous pressure will increase IOP by decreasing aqueous drainage and increasing choroidal blood volume
2-Arterial blood pressure:
Extreme changes in arterial pressure can affect IOP. Any anesthetic maneuver that affect arterial blood pressure can affect IOP such as laryngoscopy and intubation, coughing trendlenberg position.
Increase in BP--------------increase IOP
Decrease in IOP -----------decrease IOP
3-Paco2
Increase in paco2 level due to hypoventilation can increase IOP while decrease in paco2 level due to hyperventilation decrease IOP
4-Pao2
Incease pao2 has no effect on IOP while decrease in pao2 will decrease IOP.
N.B when the globe is open during certain surgical procedures or after traumatic perforation, IOP approaches atmospheric pressure. Any factor that normally increase IOP will tend to decrease intraocular volume by causing drainage of aqueous or extrusion of vitreous through the wound.
Effect of anesthetic drugs on IOP
Most anesthetic drugs lower or have no effect on IOP.
Inhalational anesthetics decrease IOP in proportion to the depth of anesthesia due to multiple causes:
- Drop in blood pressure reduce colloidal volume
- Relaxation of extraocular muscles
- Papillary constriction facilitates aqeous outflow
Intravenous anesthetics also decrease IOP with the exception of ketamine which usually raise arterial blood pressure and dose not relax extraocular muscles.
Topically administered antichlonirgic drugs result in papillary dilataion whichmay precipitate angle closure glaucoma. Premedication with systemically administered atropine is not associated with intraocular hypertension. Glucopyrrolate may provide a greater margin of safety by preventing its passage into the central nervous system.
Succinyl chlorine increase IOP by 5- 10 mmgh for 5- 10 minafter administration due to prolonged contracture of extraocular muscles. This will cause spurious measurements of IOP during examination anesthesia in glaucoma patients potentially leading to unneccssary surgery, may cause extrusion of ocular contents through an open surgical or tuamatic wound and finally abnormal forced duction test for 20 min( this maneuver evaluate the cause of extraocular muscles imbalance and may influence the type of strabismus surgery.
Systemic effects of ophthalmic drugs
Topically applied eye drops are absorbed by vessels in the conunctival sac and nasolcrimal duct mucosa.
Topically applied drugs are absorbed at a rate intermediate between absorption following iv and sc injection.
One drop of 10% of phenylephrine contains 5 mg of drug compared to 0.05 – 0.1 mg used to treat hypotension.
Echothiophate is an irreversible antichloinestrase used in the treatment of glaucoma. Topical administration lead to systemic absroptopn and reduction in plasa cholinesterase activity which will prolong duration of action of succinyl choline.
The inhibition of cholinesterase activity lasts for 3-7 weeks after discontinuation of eye drops.
Epinephrine eye drops can cause hypertension, tachycardia and vent dysrrhythmia which are potentiated by halothane.
Timolol, a non selective B blocker reduce IOP by decreasing aqeous production. It has been rarely associated with atropine resistant bradycardia, hypotension, and bronchospasm during general anesthesia.
The occulocardic reflex
Traction on extraocular muscles or pressure on the eye ball can elicit a wide variety ofmcardiac dysrhythmia ranging from bradycardia and vent ectopy to sinus arrest and vent fibrillation. It consists of afferent trigeminal and a vagal efferent pathway.
Anticholinergic medication is often helpful in preventing the occulocardic reflex. Intravenous atropine or glycopyrrolate immediately prior to surgery is more effective than intramuscular premedication.
Management of the oculcardic reflex when it occursnconsists of the following procedures:
- Immediate notification of the surgeon
- Confirmation of adequate ventilation, oxygenation and depth of anesthesia.
- Administration of iv atropine 10 ug/kg.
- Infiltration of the rectus muscle with local anesthetic.
General anesthesia a for ophthalmic surgery
Open-Eye Surgical Procedures.
Cataract extraction
Corneal laceration repair
Corneal transplant (penetrating keratoplasty)
Peripheral iridectomy
Removal of foreign body
Ruptured globe repair
Secondary intraocular lens implantation
Trabeculectomy (and other filtering procedures)
Vitrectomy (anterior and posterior)
Wound leak repair
The choice between general and regional anesthesia should be made jointly by the patient, anesthesiologist, and surgeon.
There is no conclusive evidence that one form of anesthesia is more safe than the other. However general anesthesia is indicated in uncooperative patients to prevent head movements which can prove disaterous during microsurgery or in other situations when local anesthesia is contraindicated such as high myopia, open eye injury, aphakic patient with single functioning eye.
The gools of general anesthesia include a smooth induction, stable IOP, avoidance of oculcardic reflex, a motionless field, and smooth emergence.
Premedication
Patients undergoing eye surgery may be apprehensive, particularly if they have undergone multiple procedures and there is a possibility of permanent blindness.
Pediatric patients often have associated congenital disorders (eg, rubella syndrome, Goldenhar's syndrome, Down syndrome).
Adult patients are usually elderly, with myriad systemic illnesses (eg, hypertension, diabetes mellitus, coronary artery disease). These factors must all be considered when selecting premedication.
Premedication may include:
Sedative: with dose reduction in elderly
Anticholinergic to prevent oculocardic reflex specially in children.
Antiemetics to avoid postoperative nausea and vomiting.
The choice of induction technique for eye surgery usually depends more on the patient's other medical problems than on the patient's eye disease or the type of surgery contemplated.
One exception is the patient with a ruptured globe. The key to inducing anesthesia in a patient with an open eye injury is controlling intraocular pressure with a smooth induction. Specifically, coughing during intubation must be avoided by achieving a deep level of anesthesia and profound paralysis.
The intraocular pressure response to laryngoscopy and endotracheal intubation can be somewhat blunted by prior administration of intravenous lidocaine (1.5 mg/kg) or an opioid (eg, remifentanil 0.5–1 g/kg or alfentanil 20 g/kg).
A nondepolarizing muscle relaxant is used instead of succinylcholine because of the latter's influence on intraocular pressure.
Ketamine is best avoided as it can increase IOP. The LMA can be used for ophthalmic surgery and may be associated with less coughing in emergence.
Eye surgery necessitates positioning the anesthesiologist away from the patient's airway, making close monitoring of pulse oximetry and the capnograph particularly important for all ophthalmological procedures.
Kinking of the endotracheal tube, breathing-circuit disconnections, and unintentional extubation may be more likely. Kinking and obstruction can be minimized by using a reinforced or preformed right-angle endotracheal tube.
The possibility of arrhythmias caused by the oculocardiac reflex increases the importance of constantly scrutinizing the electrocardiograph and making sure the pulse tone is audible.
In contrast to most other types of pediatric surgery, infant body temperature often rises during ophthalmic surgery because of head-to-toe draping and insignificant body-surface exposure. End-tidal CO2 analysis helps differentiate this from malignant hyperthermia.
Nitrous oxide presents a special problem in some vitriretinal procedures.N2O diffuses and cuases buble expansion with the potential of danagerous increase of IOP when sulfu hexafluoride agent is used.
N2O shold be shut off for 15min before placing sulfu hexafluoride buble and should be avoided for 7 -10 days thereafter.
Perfluoropropane is a new agent which can persist for weeks. N2O should be avoided at least for a month or until the buble is resorbed.
Extubation and emergence
Smooth emergence from general anesthesia is desirable to lessen the risk of postoperative wound dehiscence.
Coughing on ETT can be prevented by extubating patients during moderately deep level of anesthesia or administration of lidocaine 1.5 mg/kg 1 – 2 min before.
Emesis caused by vagal stimulation is a common postoperative problem, particularly following strabismus surgery. The Valsalva effect and the increase in central venous pressure that accompany vomiting can be detrimental to the surgical result and increase the risk of aspiration. Intraoperative administration of intravenous metoclopramide (10 mg in adults) or a 5-HT3 antagonist (eg, ondansetron 4 mg in adults) decreases the incidence of postoperative nausea and vomiting (PONV). Antiemetics should generally be given to patients receiving opioids and those with a history of PONV.
Severe postoperative pain is unusual following eye surgery. Scleral buckling procedures, enucleation, and ruptured-globe repair are the most painful operations. Small doses of intravenous narcotics (eg, 15–25 mg of meperidine for an adult) are usually sufficient. Severe pain may signal intraocular hypertension, corneal abrasion, or other surgical complications.
Regional anesthesia for ophthalmic surgery
Eye surgery usually requires akinesia of the eye and profound anesthesia of the operative site.
Several regional anesthetic technique have been developed that satisfy the requirement of ophthalmic surery and are generally reliable and safe.
Regional anesthesia has several advantages over general anesthesia including:
- Significant postoperative analgesia
- Infrequent nausea and vomiting
- Early ambulation and dischare of the patient.
Contraindications:
- Young patient
- Uncooperative patient
- Extreme myopia
- Open eye surgery
- Coagulopathy or warfarin therapy
Retrobulbar block
Technique: local anesthetic is injected behind the eye into the cone formed by the extraocular muscles. A blunt tip 25 gauge needle penetrates the lower lid at the junction of middle and lateral third of the orbit ( 0.5 cm medial to lateral canthus). The needle is advanced 3.5 cm towards the apex of the muscle cone. After aspiration, 2-5 ml of local anesthetic are injected and the needle is removed. Local anesthetic used varies but the most common is lidocaine and bupivacaine e.g equal volumes of bupivacaine 0.5 -7.5% + lidocaine 2-4% is used.
Additives to local anesthetics:
Hyaluronidase, a hydrolyser of connective tissue polysaccharides is frequently added to enhance the spread of local anesthetic. 5 units for each one ml local anesthetic.
Epinephrine can be added to prolong the duration of action of local anesethetic and decrease the incidence of HE due to V.C.
A succeful retrobulbar block is accompanied by anesthesia, akinesia, and abolishment of oculcephalic reflex( a blocked eye dose not move during head turning).
Extrocular pressure application help in spreading the local anesthesia--------decrease the volume--------- decrease IOP.
It is done by: gentle digital pressure and massage fot at least 20 min.
Or a pressure reducing device such as Honan s ballon, it is applied for 20 min at a pressure of no more than 35 mmgh, then the ballon is removed just before the operation.
Complications of retrobulbar block
- Retrobulbar hge
- Globe perforation
- Optic nerve atrophy
- Frank convulsions
- Oculcardiac reflex
- Acute neurogenic pulmonary edema
- Trigeminal nerve block
- Respiratory arrest
- Postretrobulbar apnea syndrome: is probably due to injection of local anesthetic into the optic sheath with spread to the cerebrospinal fluid. The CNS is exposed to high concentration of local anesthetic leading to apprehension and unconcioueness. Apnea occurs in 20 min and resolve in an hour.
facial nerve block
facial nerve block prevents squiting of the eyelids and allows placement of a lid speculum.
There are several technique of facial nerve block:
Modified vanlint: the needle is placed 1 cm lateral to the orbital rim and 2-4 ml of local anesthetic are injected deep in the periosteum just lateral to supralateral and infralateral orbit rim.
O’ Brien block: the mandibular condyle is palpated inferior to the posterior zygomatic process and anterior to the tragus of the ear. The needle is inserted perpendicular to the skin about 1 cm to the peripsteum. As the needle is withdrawn 3ml of anesthetic is injected.
Nadbath Rehman block: 12 mm, 25 gauge needle is inserted perpendicular to the skin between the mastoid process and the posterior border of the mandible. The needle is advanced its full lenghth and after careful aspiration,3 ml of anesthetic is injected. It has been associated with vocal cords paralysis, dysphagia, and respiratory stress due to close proximity to vagus and glosspharyngeal nerve.
Peribulbar Blockade
In contrast to retrobulbar blockade, with peribulbar blockade the needle does not penetrate the cone formed by the extraocular muscles. Both techniques achieve akinesia of the eye equally well. Advantages of the peribulbar technique may include less risk of eye penetration, optic nerve and artery, and less pain on injection. Disadvantages include a slower onset and an increased likelihood of ecchymosis.
A blunt 23-gauge7/8 -inch Atkinson needle is placed at the junction of the middle and lateral thirds of the lower lid just above the inferior orbital rim; 1 mL of local anesthetic is put just below the orbital septum, 3 mL at the equator, and 2 mL posterior outside the muscle cone. If no bulging is noted at the superior nasal lid area, a second injection of 2 to 3 mL is administered inferonasally.
Tenon's fascia surrounds the globe and extraocular muscles. Local anesthetic injected beneath it diffuses into the retrobulbar space. A special blunt 25-mm or 19-gauge curved cannula is used for a sub-Tenon block. After topical anesthesia, the conjunctiva is lifted along with Tenon's fascia in the inferonasal quadrant with forceps. A small nick is then made with blunt-tipped Westcott scissors, which are then slid underneath to create a path in Tenon's fascia that follows the contour of the globe and extends past the equator. While the eye is still fixed with forceps the cannula is inserted and 3–4 mL of local anesthetic is injected. Complications with the sub-Tenon blocks are significantly less than with retrobulbar and peribulbar techniques, but rare reports of globe perforation, hemorrhage, cellulitis, permanent visual loss, and local anesthetic spread into cerebrospinal fluid exist.
Several techniques of intravenous sedation are available for eye surgery. The particular drug used is less important than the dose. Deep sedation should be avoided because it increases the risk of apnea and unintentional patient movement during surgery. On the other hand, retrobulbar and facial nerve blocks can be quite uncomfortable.
As a compromise, some anesthesiologists administer a small dose of propofol (30–100 mg slowly) or a short-acting barbiturate (eg, 10–20 mg of methohexital or 25–75 mg of thiopental) to produce a brief state of unconsciousness during the regional block. Alternatively, a small bolus of an opioid (remifentanil 0.1–0.5 g/kg or alfentanil 375–500 g) allows a brief period of intense analgesia.
Other anesthesiologists, believing that the risks of respiratory arrest and aspiration are unacceptable, limit doses to provide only minimal relaxation and amnesia. Midazolam (1–2 mg) with or without fentanyl (12.5–25 g) or sufentanil (2.5–5 g) is a common regimen. Doses vary considerably among patients and should be administered in small increments. Moreover, concomitant use of more than one type of drug (benzodiazepine, hypnotic, and opioid) potentiates the effects of other agents; doses must be reduced accordingly. An antiemetic should probably be administered if an opioid is used. Regardless of the technique employed, ventilation and oxygenation must be carefully monitored, and equipment to provide positive-pressure ventilation must be immediately available.
Anesthesia for pediatric eye surgery can be considered a subspecialty of its own. Small children may need examination under anesthesia. Intramuscular ketamine sometimes can be a good choice; it can be used when intravenous access may be problematic. Some ophthalmologists prefer ketamine because it does not reduce IOP as barbiturates and deep inhaled anesthetics do.
The most common eye surgery in children is for strabismus, or misalignment of the eyes. There is generally no severe postoperative pain, but nausea and vomiting are significant 50% to 80% of the time without treatment. Droperidol 5 to 75 µg/kg seems to decrease nausea and vomiting significantly without undue delay of discharge. Ondansetron has similar effects without sedation. If forced duction testing is used to assess the muscle tightness, the surgeon should be notified if succinylcholine is used. Succinylcholine causes a tonic increase in eye muscle tone, which resolves in about 20 minutes.
Strabismus is a very common condition, and most children are otherwise healthy. There is a higher incidence of strabismus in trisomy 21 or Down syndrome, cerebral palsy, and hydrocephalus. Malignant hyperthermia and myotonic dystrophy also have been associated with strabismus. Myotonic dystrophy also is seen in patients with ptosis and cataracts.
Cataracts can be seen in children with Pierre-Robin syndrome and phenylketonuria. Patients with Marfan syndrome have a high incidence of subluxation or dislocation of the lens. Aniridia, the congenital absence of the iris, is associated with Wilms’ tumor and hypertension. Congenital glaucoma also can be seen with Sturge-Weber syndrome and with seizures and angiomas of the mouth and larynx.
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