Non obstetric surgery during pregnancy

Non obstetric surgery during pregnancy is relatively common.

The most common indications for surgery during pregnancy are either pregnancy related or pregnancy non related. Pregnancy related surgery include interventions for cervical incompetence and surgery for ovarian cyst problems.

The most common non pregnancy related indications are acute abdominal problems( most commonly appendicitis and cholecystitis), maternal trauma and surgery for malignancies.

Anaesthetists who care for pregnant patients undergoing non-obstetric surgery must provide safeanaesthesia for both the mother and the foetus.  To maintain maternal  safety the physiological and anatomical changes of pregnancy must be considered and anaesthetic techniques and drug administration modified accordingly.  Foetal wellbeing is related to avoidance of foetal asphyxia, teratogenic drugs and preterm labour.

Physiological Changes during Pregnancy

Central Nervous System Effects

The minimal alveolar concentration (MAC) progressively decreases during pregnancy—at term, by as much as 40%—for all general anesthetic agents; MAC returns to normal by the third day after delivery. Changes in maternal hormonal and endogenous opioid levels have been implicated. Progesterone, which is sedating when given in pharmacological doses, increases up to 20 times normal at term and is probably at least partly responsible for this observation. A surge in -endorphin levels during labor and delivery also likely plays a major role

At term, pregnant patients also display enhanced sensitivity to local anesthetics during regional anesthesia; dose requirements may be reduced as much as 30%. This phenomenon appears to be hormonally mediated but may also be related to engorgement of the epidural venous plexus.

Obstruction of the inferior vena cava by the enlarging uterus distends the epidural venous plexus and increases epidural blood volume. The latter has three major effects: (1) decreased spinal cerebrospinal fluid volume, (2) decreased potential volume of the epidural space, and (3) increased epidural (space) pressure. The first two effects enhance the cephalad spread of local anesthetic solutions during spinal and epidural anesthesia, respectively, whereas the last may predispose to a higher incidence of dural puncture with epidural anesthesia

Neurosurgery in children

Neurosurgery in children

Intracranial Physiology and Pathophysiology

There are a number of anatomic differences between children and adults that affect central nervous system physiology, especially intracranial pressure (ICP).

 At birth, the dura mater is covered by the calvaria, which consist of ossified plates connected by fibrous sutures and open fontanelles. The fontanelles close by approximately 10 to18 months of age but do not fully ossify until the teenage years. Thus, the infant skull is more compliant and may slowly expand in response to increasing ICP. These same structures offer a great deal of resistance to acute elevations in ICP. Infants and young children may not exhibit clinical signs of intracranial hypertension until the process is significantly advanced and the cranium can no longer accommodate a further increase in ICP.

 By the time an infant demonstrates the classic clinical signs of elevated ICP such as bradycardia, hypertension, papilledema, and pupillary changes, the disease process is likely very advanced. In contrast to adults, infants and young children may present with vague signs and symptoms such as increased head circumference, expanding sutures, bulging fontanelles, “sundowning” of eyes, lethargy, poor feeding, irritability, and possibly lower motor deficit.

 After ossification of the fontanelles, for a time, children may be more vulnerable to brain injury from increased ICP because of a relatively higher brain tissue to blood and cerebrospinal fluid intracranial volume than in the adult.

The limits of autoregulation are also different in infants and children. In adults, normal ICP ranges between 8 and 15 mmHg, whereas in infants, it may be as low as 2 to 4 mmHg. The cerebral autoregulation limit is shifted to a significantly lower value of mean arterial blood pressure (20 to 60 mmHg). The “margin of safety” may be narrower because infants are less able to compensate for the changes in blood pressure. Global cerebral blood flow (CBF, measured as ml/min/100 g of brain tissue) in children is greater than in adults, but in infants and premature babies, it is lower. The lower limit of CBF needed to sustain neuronal integrity is unknown in these patients. In infants with pathologic conditions resulting in a shift of the intracranial compliance curve to the right, cerebrospinal fluid production alone may be a significant contributor of increased ICP. Infants are at risk for ischemia when mean arterial pressure is low, whereas systemic hypertension may result in intraventricular hemorrhage; therefore, large fluctuations in systemic blood pressure may be deleterious. The response to hyperventilation may, also, be exaggerated and ischemia may ensue with very low PCO2 levels (less than 20 mmHg).

Twin-to-twin transfusion syndrome (TTTS)

Ain Shams Journal of Anesthesiology                                         Vol 4-1; Jan 2011
99
Twin-to-twin transfusion syndrome (TTTS)
 
Mohammed Abdel-Galil Sallam MD
Department of Anesthesiology, Intensive Care, and Pain Management, Faculty of
Medicine, Ain-Shams University, Cairo, Egypt
TTTS only occurs in monozygotic
(identical) twins with a monochorionic
placenta. It is the result of an
intrauterine blood transfusion from one
twin (donor) to another twin
(recipient). The donor twin is often
smaller with a birth weight 20% less
than the recipient’s birth weight. The
donor twin is often anemic and the
recipient twin is often plethoric with
hemoglobin differences greater than 5
gm/dL. The blood transfusion from the
donor twin to the recipient twin occurs
through placental vascular anastomoses.
The most common vascular anastomosis
is a deep, artery-to-vein anastomosis
through a shared placental cotyledon.
The clinical feature es of TTTS are
the result of hypoperfusion of the donor
twin and hyperperfusion of the recipient
twin.

Some Games on Anaesthetist.com

Some Games on Anaesthetist.com

Asthma Cardiac Arrest

Asthma Cardiac Arrest

In the early 1990’s at  the Alfred Hospital in Melbourne a young man was admitted in extremis with severe asthma. He had had many previous admissions some requiring ICU. He was intubated and ventilated, and given salbutamol and adrenaline.

However he went into asystole and was given all resuscitation measures but a rhythm could not be established. His pupils became dilated and fixed and further resuscitation was considered futile.

He was disconnected from the self-inflating bag and most of the staff left the room. After a few minutes a nurse noted that the patient had developed sinus rhythm. Staff were recalled and ventilation was recommenced.

However shortly afterwards he became pulseless  and again went into asystole. After some time resuscitation was again declared unsuccessful. Following disconnection from the breathing system the patient again developed a rhythm and pulses. Each subsequent time he was ventilated the same thing happened.

The staff realized that IPPV was causing the problem. Gentle ventilation with a slow respiratory rate was continued. The patient subsequently made a full recovery. This cases was written up in the journal “Anaesthesia and Intensive Care” in 1991 Vol 19 pp 118-121. Similar cases have since been published.

The problem here was gas trapping leading to high intrathoracic pressure which prevented venous return to the heart and resulted in cardiac arrest.

It is now appreciated that care must be taken with ventilation in asthma to allow ample time for expiration. A low respiratory rate of perhaps 6 breaths per minute should be combined with a long I:E ratio (say 1:6) to prevent gas trapping. Some level of “permissive” hypoxia and hypercarbia  is now considered to lead to better outcomes in ventilated asthmatic patients in preference to gas trapping.

There is not much point having oxygen in the lungs if there is no cardiac output to deliver it to vital organs.

Take Home Message:

Avoid high intra-thoracic pressures and gas trapping in ventilated patients with asthma.

This also applies to shocked patients where blood is returning to the thorax at very low pressure.

 source: http://www.anaesthesiacases.com.au/cases/asthma_cardiac_arrest

Anaesthesia Points to Remember

Beware of conus injuries from needling the spinal cord during spinal anaesthesia. It can lead to lifelong disability and pain. Once you insert your spinal needle more than one space above a line joining the iliac crests then the risks start to escalate.

Maintain adequate levels of blood pressure during anaesthesia. Hypotension  under anaesthesia  continues to be associated with increased morbidity and mortality. Patient age and co-morbidities should influence the minimum acceptable blood pressure. 

The recommended dose of morphine for an IV PCA  should not be greater than 1 mg with a 5 minute lockout, except in opiate dependent patients.

There is no point giving a test dose of antibiotic IV unless you perform minute dilutions into one litre of crystalloid and run it into the patient slowly.

Blood needs to be carefully checked to ensure the correct patient is receiving the correct blood. Errors continue to occur. Mismatched blood transfusion carries a high mortality rate.

When injecting significant amounts of LA it is recommended to have patients awake and communicative to reduce the likelihood of LA toxicity

Aspiration prior to injection does not rule out being intravascular (the side of the vessel wall can be sucked against the bevel of the needle).

Slow injection of LA is essential while maintaining communication with the patient: “Tell me if you are experiencing anything unusual”.

Longer acting LA’s such as bupivacaine  and ropivacaine have a higher incidence of LA toxicity than shorter acting ones such as lignocaine or prilocaine.

LA toxicity with mortality and major morbidity continues to occur.

Laryngeal tumours can create major airway difficulties for anaesthesia with airway obstruction and bleeding

Patients with laryngeal tumours ideally should have an MRI prior to anaesthesia.

Beware of gas trapping with IPPV in patients with respiratory conditions such as asthma and cystic fibrosis. This can lead to cardiovascular collapse. Such patients require reduced respiratory rates and longer I:E ratios to allow sufficient time for gas to be exhaled.

In patients with gastric outlet obstruction be prepared for regurgitation of large volumes of gastric fluid or blood.

Naloxone can precipitate massive sympathetic response with pulmonary oedema. Giving divided doses may diminish this effect.

Take care not to have malleable stylets protruding out the end of ETTs as they can also cause tracheal damage.

Jet ventilation must be used with considerable caution as surgical emphysema and pneumothoraces have been frequently reported. Care must be taken to ensure the upper airway is not obstructed. Gas needs to be able to get out as well as get in.

TIVA continues to be associated with awareness under anaesthesia.

Gas insufflation at laparoscopy can cause asystole or profound bradycardia. Careful monitoring is required. Treatment may require allowing the gas to escape rapidly.

Negative pressure pulmonary oedema may occur following emergence from anaesthesia in younger patients. CPAP or IPPV will usually be required.

Syringe swap continues to cause problems. Take extra care with muscle relaxants and vasopressors.

If your patient is hypotensive consider anaphylaxis, particularly if you have given muscle relaxants or antibiotics. There are many case reports of patients receiving  significant doses of metaraminol and ephedrine prior to anaesthetists starting definitive treatment of anaphylaxis with adrenaline.

source: http://www.anaesthesiacases.com.au/opinion/topics/anaesthesia_points_to_remember

"Take a pencil and paper," the teacher said, "and write an essay with the title 'If I Were a Millionaire.'"

Everyone but Philip began to write furiously. He just leaned back in his chair and folded his arms.

"What's the matter," the teacher asked. "Why don't you begin?"

"I'm waiting for my secretary," he replied