THE PATIENT WITH PULMONARY HYPERTENSION

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.

Neuroleptic Malignant Syndrome

The Indian Anaesthetists’ Forum – (http://www.theiaforum.org)                    Online ISSN 0973-0311
January 2010(4)
Agrawal P,Agrawal A, Singh I: Neuroleptic Malignant Syndrome and Anaesthesia : A Case Report  1
Neuroleptic Malignant Syndrome and Anaesthesia: A Case Report
1. DNB Resident Presently working as Senior Resident, JPNATC, AIIMS, New Delhi
2. Consultant, 3. Head of the Department
Department of Anaesthesiology and Intensive Care
Jaipur Golden Hospital, Rohini, New Delhi.
Correspondence: Pramendra Agrawal (pramendraagrawal@yahoo.com)  
About the Author: Dr Pramendra Agrawal passed
DNB in Anaesthesiology in the year 2008. He is
presently working as Senior Resident in Jai Prakash
Narayan Apex Trauma Centre, All India Institute of
Medical Sciences [AIIMS], New Delhi, India. His field
of interests include trauma care, regional interventional techniques and intensive care.
Neuroleptic Malignant Syndrome (NMS) is a life threatening, neurological disorder most
often caused by an adverse reaction to neuroleptic or anti psychotic drugs. We report a case
of Neuroleptic Malignant Syndrome who was posted for an incidental surgery and its
anaesthetic management.
Key Words: Neuroleptic Malignant Syndrome, anti psychotics, hyperthermia
Neuroleptic Malignant Syndrome (NMS) is a rare but  potentially life threatening
idiosyncratic reaction to neuroleptic drugs. It causes hyperthermia, muscular rigidity, altered
mental status, elevated creatine phosphokinase (CPK) and autonomic dysfunction. The
underlying pathological abnormality is thought to be the central dopamine D2 receptor
blockade or dopamine depletion in the hypothalamus, nigrostriatal and spinal pathways.
The condition shares many features with the serotonin syndrome and malignant
hyperthermia. Anaesthesia for an incidental surgery in such a patient poses unique
challenges to an anaesthesiologist.  
Case Report: An 18 year old male, a known case of Bipolar mood disorder on antipsychotics
was admitted to our Intensive Care Unit with complaints of high grade fever (106F) for 2
days, agitation and involuntary movements for 8 days and vomiting with altered sensorium
for 1 day. Patient was immediately intubated to protect his airway, intensive measures to
bring down temperature commenced and investigations including haematological, biochemical, brain imaging and cerebrospinal fluid sent for evaluation. Investigations revealed:
 elevated liver enzymes (SGOT 477 IU/l, SGPT 190  IU/l);
progressively increasing Creatine Kinase (1004; 2040; 3270; 39794 U/l), Serum Creatinine
(1.3; 1.5; 1.8 mg/dl) and Serum K+ (4.8, 4.9, 5.5 meq/l). Computed tomography of brain and
cerebrospinal fluid examination were normal.  So a  diagnosis of neuroleptic malignant
syndrome was made.  All antipsychotic medications were then stopped.  Tab. Bromocriptine
1.25 mg thrice daily and Tab. Alprazolam 0.25 mg four times daily were started and other
intensive care measures continued. Patient was gradually weaned off ventilator support and
extubated on 6th day.
Unfortunately patient developed a bed sore on the buttock which needed a flap
cover He was posted for surgery on 15th day of admission. A pre-anaesthetic check up
revealed a responsive patient, hypertonia present in all limbs and restricted mouth opening
(just 2 fingers due to hypertonia). Investigations  revealed elevated CPK 829 U/l, S. K+ 4.9
meq/l, INR = 1.54; rest of examination and investigations were within acceptable limits.
Anaesthetic management included avoidance of following drugs perioperatively: Inj.
droperidol, succinylcholine, prochlorperazine, promethazine and metoclopramide. Patient
received premedication with alprazolam 0.25 mg at 10 p.m. before the day of operation and
at 6 a.m. on day of surgery. Consent taken and patient shifted to operation theatre. Drip
started with 16 G intravenous cannula and standard  monitoring established. Fentanyl 1.5
µg/kg and midazolam 1 mg IV was administered. Anaesthesia induced by thiopentone
sodium 4 mg/kg IV slowly, after pre-oxygenation or  5 minutes and adequacy of mask
ventilation confirmed, muscle paralysis achieved with atracurium 0.5mg/kg. Airway secured
with 34Fr cuffed armoured endotracheal tube orally and anaesthesia maintained with 50%
of O2 + N2O + Isoflurane < 0.4%, fentaynl was used for analgesia and atracurium for muscle
paralysis assisted by neuromuscular monitoring. Surgery was conducted in prone position;
procedure lasted 2½   hours during which 2 units of whole blood, 2 units of FFP and 1.5 litres
crystalloid were infused. Patient remained haemodynamically stable throughout procedure.
At end of surgery, neuromuscular blockade was reversed with neostigmine and
glycopyrrolate. Trachea was extubated in prone posture itself as requested by surgeons to
avoid pressure on flap after patient was awake; Ondansteron 4mg IV was used as
antiemetic.
Post operatively patient was shifted to post anaesthesia care unit with O2
supplementation and then towards after 2 hrs. Patient was discharged from hospital on 7th
post operative day with psychiatry referral.
Discussion: Neuroleptic Malignant Syndrome (NMS) was first described by Delay et al during
early trials of haloperidol. The incidence is estimated to range from 0.02–2.4% with The
Diagnostic criteria are:
• Administration of neuroleptics
• Hyperthermia (> 38oC)
• Muscle rigidity
• Five of following: mental status change, tremor, tachycardia, incontinence, labile
blood pressure, metabolic acidosis, tachypnoea/hypoxia, CPK elevation,
diaphoresis/sialorrhea, leukocytosis.
• Exclusion of other central and systemic causes of hyperthermia.
 Although NMS has a variable onset and sometimes evolves rapidly, rigidity and
altered mental status usually occur early, followed by autonomic changes and
hyperthermia. No laboratory tests are pathognomonic of diagnosis. Serum creatine kinase
is frequently elevated reflecting rhabdomyolysis, with resultant risk of myoglobinuric renal
failure. CT scan brain and cerebrospinal fluid examination and sepsis evaluation are negative
in NMS and allow for   the exclusion of other causes of fever and neurological deterioration.
Other frequently described laboratory abnormalities include metabolic acidosis, hypoxia,
low serum iron, electrolyte abnormalities, elevated serum catecholamines and
coagulopathies
Differential Diagnosis of NMS: Infectious encephalitis4,5, structural lesion of brain, rare
cases of status epilepticus6, lethal catatonia7, heat stroke, endocrinopathies, drugs,
autoimmune disorders, thyrotoxicosis, phaeochromocytoma, malignant hyperthermia,
serotonin syndrome. Volatile anaesthetics and succinylcholine are associated with
malignant hypertherma during surgery, which can be confused with NMS if neuroleptics are
administered

The basic management of NMS remains risk reduction, early diagnosis, cessation of
neuroleptic medications and institution of Intensive, medical and nursing care.
Benzodiazepines, bromocriptine, amantadine or other dopamine agonists may be a
reasonable next step in patients with moderate symptoms of NMS. Dantrolene may be
beneficial in cases of NMS with extreme rigidity and hyperthermia. Electro convulsion
therapy (ECT) is used if NMS is refractory to other measures or who remain psychotic after
NMS   is resolved. Since a common pathophysiology has been suggested between NMS and
malignant hypertherima (MH) the possibility that patients with a history of NMS may be
vulnerable to developing MH is an important factor when considering general anaesthesia,
especially succinylcholine administration. To date, there is no report in the literature of
(MH) as a complication of ECT in NMS patients. However, until the association between
NMS and MH is conclusively disproved, careful metabolic monitoring of general anaesthesia
is necessary.
Conclusion: Neuroleptics are highly effective medications that have achieved wide spread
use in medicine and psychiatry. However they have been associated with NMS in about 0.2
percent of patients. Awareness of diagnosis, cessation of medications, early medical
intervention and consideration of specific remedies can reduce morbidity and mortality
when NMS occurs. This case report has been published to increase familiarity with the
diagnosis and management of this unusual but fascinating drug reaction and anaesthetic
management of a incidental surgery in a patient of NMS.
References:  
1. Delay J., Pichot P., Lemperiere T, Elissade B., Peigne F. Un neuroteptique majeur non
phenothiazine et non reserpinique, L’haloperidol dans Le traitment des psychoses.
Annales Medico-Psychologique 1960 ; 118:145 – 152.
2. Ananth J Parameswaran S., Gunatilake S. et. al.; Neuroleptic malignant syndrome
and a typical antipsychotic drugs. J. Clin Psychitary 2004 Apr: 65 (4): 464- 70.  
3. Velamoor VR, Normal RM, Caroff SN, Mann SC, Sullivan KA, Antelo RE. Progression of
symptoms in Neuroleptic Maligant Syndrome. Journal  of Nervous and Mental
Disease : 1994 ; 182: 168 – 173.
4. Caroff SN, Mann SC. McCarthy M, Naser J., Rynn M, Morrison M. Acute infectious
encephalitis complicated by Neuroleptic Malignant Syndrome. Journal of Clinical
Psychopharmacology 1998 ; 18 : 349-351
5. Caroff SN, Mann SC, Gliatto MF, Sullivan KA, Campbell EC. Psychiatric Manifestations
of acute viral encephalitis. Psychiatric Annals 2001: 31; 193-204.
6. Caroff SN, Mann SC, Neuroleptic Malignant Syndrome. Medical clinics of North
America 1993; 77: 185-202
7. Mann SC, Caroff SN, Bleier HR, Welz WKR, Kling MA, Hayashida M. Lethal catatonia ;
1986; 143: 1374 – 1381
8. Keck PE Jr. Arnold LM. The serotonin syndrome. Psychiatric Annals 2000 : 30 : 333 –
343
9. Caroff SN, Rosenberg H., Mann, Campbell EC, Gliatto MF, Sullivan KA, Neuroleptic
Malignant Syndrome in the perioperative setting. American Journal of
Anesthesiology 2001,: 28 ; 387 – 393
10. Davis JM, Caroff SN, Mann SC. Treatment of neuroleptic malignant syndrome
Psychiatric Annals 2000; 30: 325 – 331.  
11. Caroff SN, Mann SC, Keck PE, Jr. Specific treatment of the neuroleptic malignant
syndrome. Biological Psychiatry 1998; 44: 378 – 381.   The Indian Anaesthetists’ Forum – (http://www.theiaforum.org)                    Online ISSN 0973-0311
January 2010(4)
Agrawal P,Agrawal A, Singh I: Neuroleptic Malignant Syndrome and Anaesthesia : A Case Report  5
12. Denborough MA, Collins SP, Hopkinson KC. Rhabdomyolysis and malignant
hyperpyrexia. Br Med J 1985; ii: 1878
13. Tollefeson G. A case of neuroleptic malignant syndrome in vitro muscle comparison
with malignant hyperthermia J. Clin Psychopharmacol 1982; 2: 266 – 70  

pediatric trauma

Management principles of pediatric trauma patients

Management principles of pediatric trauma patients are similar to those of adults, but modified according to the age group of the child. Children are not just small adults. Their unique, developing psychologic, anatomic, and physiologic characteristics pose special challenges to anesthesiologists and the entire trauma care team. Optimal management of the pediatric trauma patient depends on adequate knowledge and

understanding of these unique characteristics.

INITIAL ASSESSMENT AND MANAGEMENT

Primary Survey

The main goal of the primary survey is to rapidly find all potentially life-threatening injuries to prioritize management for efficient resuscitation and achieve hemodynamic stability. This requires immediate assessment of the “ABCDEs” of the Advanced Trauma Life Support (ATLS) protocol and constant reevaluation of the adequacy of resuscitation strategies.

Airway with C-Spine Control

Evaluation of the airway in an injured child can be complex. Injury to the airway or nearby structures may distort normal anatomy and render mask ventilation and tracheal intubation difficult.Preexisting conditions thatmay complicate emergency

airway management include congenital abnormalities, such as micrognathia (mandibular hypoplasia), macroglossia, and cleft palate and the presence of obstructive sleep apnea with or without obesity.

Inspection of the airway includes the face, mouth, mandible, nose, and neck. Look for edema, foreign bodies, secretions, blood, loose or missing teeth, and fractures of the jaw, mandible, and cervical spine. Any trauma victim, especially one with a closed-head injury, is presumed, until proved otherwise, to have cervical spine (C-spine) injury and a full stomach.

C-spine precautions

should be maintained and techniques that minimize the risk of pulmonary aspiration should be taken at all times.

Healthy neonates and young infants have large heads, including prominent occiputs relative to body size, so that, in the supine position, the infant neck is naturally flexed on the chest and the supine infant headmay be flexed on the neck]. This has several important implications.

The natural head and neck flexion of the obtunded or sedated young infant often results in significant airway obstruction that may be relieved by gently lifting the chin up and forward (anteriorly) to slightly extend the head on the neck. Otherwise, an

oral airway can be inserted with no relative movement of head and neck. In suspected C-spine injury, a more neutral, straight head and neck position should be achieved by placing a blanket or pad under the supine infant or young child’s torso.

Neonatesandyounginfants areobligate nose breathers until three to five months of age so that any secretions or blood in their relatively narrow nasal passages can lead to airway obstruction.

The larynx in infantsandchildren ismore cephalad, approximately at the level of the C3–C4 vertebrae in infants compared with the C5–C6 level in adults. This may give the impression that the infant larynx is more anterior during direct laryngoscopy.

The length of the trachea is only 4–5 cm in infants and approximately 7 cm by 18 months of age, so right mainstem intubation or ETT dislodgement can occur with correspondingly small movements of the infant’s head. extubation.When choosing the appropriately sized ETT, keep in mind that in children less than 5 years old, the narrowest part of the upper airway is at the level of the cricoid cartilage, not at the glottis, as in adults. The size of the ETT appropriate for the patient’s age may

be estimated by comparing the tube size with that of the infant or child’s fifth finger, or by using the formula: ETT tube size (diameter in mm) = 4 + (1/4) age .

An air leak around the ETT at 15–20 cmH2Opressure and easy passage of the tube into the trachea clinically suggests that the ETT size is appropriate. The following formula may be used as a guide to determine the appropriate depth of the ETT placement (in centimeters from lips to tip of ETT) for children older than 2 years: 13 + (1/2) age); for under 1 year old: 8 + weight in kilograms [20].

The appropriate depth of ETT insertion may also be approximated bymultiplying the internal diameter (millimeters) of the ETT by 3.

Indications for Endotracheal Intubation

a. Loss of consciousness or altered level of consciousness with inability to protect the airway

b. Inability to maintain patency of airway or clear secretions

c. Provide positive pressure ventilation and adequate oxygenation

d. Significant burn with airway injury.

Different Methods Of Intubation In Difficult Situations

Stiff Person Syndrome

Stiff Person Syndrome and Anesthesia: Case Report

1. Jans Bouw, MD*, 
2. Karin Leendertse, MD*, 
3. Marina A. J. Tijssen, MD PhD†and 
4. Misa Dzoljic, MD PhD*

+Author Affiliations

1. *Departments of Anesthesiology and †Neurology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

1. Address correspondence and reprint requests to J. Bouw, MD, Department of Anesthesiology, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands. Address e-mail toj.bouw@amc.uva.nl.

 

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Abstract

IMPLICATIONS: This case report describes the successful perioperative management of a patient with a rare and disabling neurologic disorder, the stiff person syndrome. The patient had a delayed emergence despite apparent full reversal of neuromuscular blockade. We suggest an interaction between the GABAergic effects of baclofen and volatile anesthetics as a possible cause.

Stiff person syndrome (SPS) is a rare and disabling neurologic disorder characterized by muscle rigidity and episodic spasms that involve axial and limb musculature (1–3). The literature points toward an autoimmune disorder resulting in a malfunction of γ-aminobutyric acid (GABA)-mediated inhibitory networks in the central nervous system (4). Anesthetic implications are less well described. We report a case of prolonged hypotonicity after general anesthesia in a patient with SPS and discuss the possible anesthetic interactions.

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Case Report

A 62-yr-old woman (height, 1.70 m; weight, 61 kg) was scheduled for resection of a colon carcinoma. Her medical history revealed hypothyroidism, vitamin B12 deficiency, and SPS. This syndrome started with low back pain, which rendered her unable to walk. She was experiencing stiffness, involuntary jerks, and painful cramps. Neurological examination revealed extreme hypertonia of the body and proximal legs, with intercurrent, painful spasms. Reflexes were symmetrical without Babinski signs. Laboratory findings showed positive glutamic acid decarboxylase (GAD) and negative amphiphysin antibodies. The patient was successfully treated with baclofen and diazepam. Subsequently, prednisone as immunosuppressive therapy was started. The stiffness diminished, and the patient was able to walk unaided. The neurological examination was unremarkable, except for a slight stiffness in the legs. Her medication at admission was prednisone 20 mg once a day, baclophen 12.5 mg twice a day (daily dose = 25 mg), diazepam 7.5 mg twice a day (daily dose = 15 mg), levothyroxine 25 μg once a day, and vitamin B12 injections. Her medical history included urological and gynecological surgery under general anesthesia before she experienced SPS.

No premedication was given. Anesthesia was induced with propofol (2.5 mg/kg) and sufentanil (0.25 μg/kg). After the administration of atracurium (0.6 mg/kg), the trachea was intubated, and anesthesia was continued with isoflurane (0.6–1.0 vol%) and oxygen/air for the duration of the procedure. Cefuroxime 1500 mg, clindamycin 600 mg, and dexamethasone 10 mg were administered IV. In the following 2 h, additional atracurium (35 mg), sufentanil (10 μg), and morphine (8 mg) were administered. At the end of the procedure, which was uneventful, neuromuscular monitoring showed four strong twitches. Although the patient was responsive, she could not open her eyes, grasp with either hand, or generate tidal volumes beyond 200 mL. Neostigmine 2 mg (0.03 mg/kg) and glycopyrrolate 0.2 mg did not alter the clinical signs of muscle weakness.

The patient was sedated with propofol 5 mg · kg⁻¹ · h⁻¹ and further mechanically ventilated in the recovery room. After 1 h, the sedation was stopped and mechanical ventilation was terminated. At that time, baclofen 12.5 mg was administered into the gastric tube. Two hours later she was in a good clinical condition, and her trachea was extubated.

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Discussion

SPS was recognized as a distinct entity in 1956 by Moersch and Woltman (5). An autoimmune pathogenesis is suspected because of the presence of antibodies against GAD, the rate-limiting enzyme for synthesis of the inhibitory neurotransmitter GABA, and the association of the disease with other autoimmune conditions such as diabetes and thyroiditis (6,7). Loss of inhibition from higher centers causes hyperactivity of the γ-motor neuron system and subsequent progressive muscle rigidity. Patients with SPS have high immunoglobulin G/anti-GAD-65 antibodies, which are synthesized intrathecally and seem to impair the in situ synthesis of GABA (8,9). Two types of drugs have been applied: drugs that enhance GABA activity and immunosuppressing drugs. Diazepam, which increases the frequency of opening of the GABA_A receptor and leads to hyperpolarization, is the initial treatment of choice at daily doses up to 200 mg. Intrathecal or oral baclofen may improve the physical symptoms just like prednisone, plasmapheresis, and large-dose IV immunoglobulin (10).

In our case, several drugs could have caused muscle weakness (11). Initially atracurium could be suspected. Computer-simulated pharmacokinetic analyses suggested that plasma concentrations were far less than therapeutic levels. The same can be said for opioids, fentanyl, and morphine (Fig. 1) (12–15). In the recovery room while the patient was still ventilated, it showed a diazepam serum concentration of 0.317 mg/L (therapeutic range, 0.125–0.75 mg/L). Because IV drugs can be excluded as causing muscular weakness, perhaps volatile anesthetics were the cause. In the case report by Johnson and Miller (10), muscle weakness was observed only when baclofen was combined with inhaled desflurane or isoflurane. Delayed arousal and muscle weakness were also described, unrelated to SPS, in a patient receiving baclofen and undergoing anesthesia with isoflurane 1% (16). In addition, recent animal studies show that baclofen enhances volatile anesthetic-induced anesthesia (17). Perhaps the complicated course of recovery was most due to the interaction between isoflurane and baclofen causing muscle weakness.

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Figure 1. Chart showing three different drugs given during the procedure. Time 0 represents the start of the procedure, which ended after 150 min. The serum concentrations of sufentanil and atracurium, although given in different units, can be seen on the left axis, and the right axis represents serum concentrations of morphine. It is noteworthy that after the initial intubation dose of atracurium, three doses (5, 10, and 20 mg) were given during the procedure.

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We thus conclude that the prolonged muscle relaxation can be explained by the enhancement of general anesthetics via GABA_B action on synaptic transmission (17). This case demonstrates a potential danger in combining baclofen with volatile anesthetics in patients with SPS.

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ANAESTHESIA FOR DAY SURGERY

THE HONG KONG COLLEGE OF ANAESTHESIOLOGISTS P5 February 1993

Reviewed Feb 2002

GUIDELINES FOR DAY CASE SURGERY

GUIDELINES ON ANAESTHESIA FOR DAY SURGERY

1. GENERAL COMMENTS

Safety of anaesthesia must not be compromised by financial or other expediency,

to the detriment of those who, by definition, are fitter than the majority of the

population.

2. FACTORS AFFECTING CHOICE OF PATIENT

2.1 Patients should be ASA (American Society of Anaesthesiologists) grade I or II. Exceptionally ASA grade III may be accepted.

2.2 Children, (who should be over six months of age), must be accompanied by parents/guardians at all relevant times.

2.3 Patients should reside within easy access to the surgical facility.

3. PREANAESTHETIC ASSESSMENT

3.1 Every patient must have a preanaesthetic assessment by an anaesthesiologist, preferably by the one who will administer the anaesthetic.

3.2 This assessment may be made in a hospital, clinic or in the day case centre.

3.3 When appropriate, the results of investigations, eg. chest X-ray, electrocardiogram, serum electrolyte and urea concentrations, and urinalysis, must be available to the assessing anaesthesiologist.

3.4 Acceptance for day case anaesthesia should be refused if the patient is unfit, appropriate medical information is lacking or the likelihood of complications is high.

4. PREANAESTHETIC INSTRUCTIONS

4.1 Proforma should be prepared to advise the patient/guardian of details about fasting time, reporting time and admission procedures.

4.2 In the case of a minor, a parent/guardian must accompany the patient to elaborate, if necessary, on the medical history (vide 3.1), and provide assistance, if required during induction and/or recovery.

4.3 Signed consent for the proposed procedure must be obtained from the patient or guardian and a preoperative leaflet discussed and handed out.

5. STAFFING

5.1 The anaesthesiologist must be provided with a dedicated and appropriately trained assistant.

5.2 There must be adequate assistance for the transporting and positioning of patients.

5.3 A qualified anaesthesiologist should be immediately available when anaesthesia is given by a trainee.

6. FACILITIES

6.1 The day surgery centre must have facilities which conform with the guidelines issued by the College, in particular :-

Recommended minimum facilities for safe anaesthetic practice in operating suites (T2).

Guidelines for monitoring in anaesthesia (P1).

Guidelines for postanaesthetic recovery care (P3).

6.2 Easy access to transport facilities is important.

7. SURGICAL CASE SELECTION

7.1 The scope and nature of surgery must be agreed by the surgeon and anaesthesiologist responsible for the day surgery in the centre.

7.2 Patients who might require blood transfusion, suffer excessive postoperative discomfort, or who are unlikely to be fit to be discharged home on the same day, are unsuitable for day surgery.

7.3 Patients living in single accommodation or who are unable to provide a responsible person to oversee their welfare for the first 24 hours cannot be accepted for day surgery.

8. POSTOPERATIVE RECOVERY

8.1 Patients must be observed and recovered by appropriately trained staff prior to discharge.

8.2 There should be a record of recovery to include conscious state, orientation,

sensory and motor function (including locomotion), pulse rate, blood pressure, and any postoperative pain.

9. DISCHARGE

9.1 Verbal and written instructions must be given to the patient and/or guardian prior to discharge with particular reference to :-

9.1.1 Immediate action in the event of complications, and

9.1.2 Whom to contact (with telephone number).

9.2 The patient must be advised verbally and in writing, that, in the first 24 hours

postoperatively, he/she must NOT :-

9.2.1 Drive or operate machinery.

9.2.2 Cook.

9.2.3 Work or make important decisions.

9.2.4 Drink alcohol.

9.2.5 Take any medication except that approved by the day case centre.

9.3 The patient must be escorted home by a responsible adult by private transport. In

the case of a minor, the responsible person attending the child during transport

should not be the driver.

9.4 If the discharge criteria are not met, the patient must be admitted.

9.5 The anaesthesiologist who gave the anaesthetic, in conjunction with the operator

and the nursing officer in charge of the day case centre, is responsible for the

discharge of the patient in accordance with agreed protocols.

view from Tahrir square