Office emergencies

Published on 09/05/2017 by admin

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Last modified 09/05/2017

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Figure 9-1

I-gel® spraglottic device (with permission from Intersurgical Ltd, Wokingham, Berkshire, United Kingdom).

The 2010 American Heart Association (AHA) guidelines on cardiopulmonary resuscitation suggest that continuous monitoring of expired carbon dioxide is mandatory if the patient is being ventilated via an endotracheal tube or supraglottic airway (Figure 9-2).[2]

Figure 9-2

CO2 detector.

In addition to capnography, monitoring should include pulse oximetry, ECG, and noninvasive blood pressure measurement.

Staff must be trained and regularly updated in the management of emergencies and the use of drugs, equipment and monitoring required. The use of protocol based drills enables health-care providers to become proficient in the skills required. Teamwork practice in the actual work environment is important. The evidence that higher fidelity simulation training in the management of emergencies improves patient outcomes does not yet exist. As emergencies are rare, easily accessible checklists and algorithms of care are recommended and have been shown to impact patient outcome.[3]

Finally it is crucial that there is a validated transfer protocol in place. The likely time for transfer, the means by which it occurs, the destination and the staff who will be involved should be determined in advance. Protocols, documentation, and equipment must be agreed upon by transferring and receiving parties. The unexpected emergency department arrival of a patient suffering a complication from an office based procedure, without prior communication and planning, should be viewed as a failure of care.

Cardiac arrest


Ischemic heart disease is the leading cause of death among women in the United States and is associated with increasing levels of obesity, smoking, hypertension, diabetes, and hypercholesterolemia;[4] 60% of deaths from ischemic heart disease are due to sudden cardiac arrest. Many of the complications discussed in this chapter may lead to cardiac arrest. The more rapidly a return of spontaneous circulation occurs, the more likely the outcome will be good; up to 30%–40% survival is thought to be possible with prompt cardiopulmonary resuscitation (CPR).

Survival after out-of-hospital cardiac arrest is poor with only 50% victims receiving bystander CPR. Survival in the office setting should approach that of hospital in-patients. The American Society of Anesthesiologists guidelines already require that personnel trained in advanced life support are present whenever patients receive sedation/anesthesia.[5]

The components that lead to a successful outcome have been termed the “chain of survival” and include early recognition and summoning help, early CPR with effective chest compressions, early defibrillation if indicated, effective advanced life support and effective post-resuscitation care.


Prompt recognition is vital. The patient is unresponsive since cardiac arrest leads to unconsciousness within 15–30 seconds. Pulses are absent and abnormal gasping respiration or apnea is present. The pupils will usually be dilated. Seizures may occur. The 2010 AHA guidelines recommend summoning help and beginning CPR on an unresponsive patient who is breathing abnormally or apneic, as time can be wasted trying to palpate for a pulse. The advice to “look, listen, feel” has been withdrawn.

Initial management

Initial management follows the AHA basic life support algorithm (Figure 9-3).[6] Chest compressions should start before airway maneuvers or rescue breaths. The emphasis is on effective compressions with minimal interruptions. The ratio of compressions to breaths is 30:2 with a rate of 100 compressions per minute. Compression only resuscitation is an option for adults not suffering drowning. As long as the airway is patent, air will be drawn into the lung and the oxygen (21%) will be sufficient to address hypoxemia.

Figure 9-3

American Heart Association basic life support algorithm.

Securing the airway allows the patient to be ventilated without having to halt compressions. Attempts to secure the airway, however, must not lead to compression interruption. As soon as possible, an AED should be attached. If a shockable rhythm is detected the 2010 guidelines suggest a single shock immediately followed by compressions. Compressions should cease only once the pads have been attached to the chest and the machine charged to further minimize interruption to compressions.

Intravenous access should be secured as early as possible in order to administer epinephrine 1 mg every 3–5 minutes as per the advanced life support (ALS) algorithm (Figure 9-4). If ventricular fibrillation persists after three shocks amiodarone 300 mg should be administered. Atropine is no longer recommended. If intravenous access is impossible the interosseous route can be used. The tibial and humeral sites are usually accessible and fluids as well as drugs can be administered by this route when the equipment is available (Figure 9-5). Reversible causes of cardiac arrest that may arise and can be treated in the office setting include hypoxia, hypovolemia (hemorrhage), and toxins (e.g., local anesthetic toxicity).

Figure 9-4

American Heart Association advanced life support algorithm.

Figure 9-5

Ezio interosseous drill.

Compressions and defibrillation should be continued during transfer and compressions should not cease until there are clear signs of return of spontaneous circulation.


As mentioned previously, continuous waveform capnography is recommended in ventilated patients. Return of spontaneous circulation will be indicated by an increase in expired CO2. Blood pressure should be measure and oxygen saturations measured. A 12-lead ECG should be performed, and blood taken for biochemistry and full blood count.

Acute coronary syndrome


Acute coronary syndrome (ACS) refers to a diagnosis of myocardial infarction or unstable angina. Myocardial infarction (MI) may be further subdivided into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). NSTEMI and unstable angina occur as a result of the development of thrombus on an atheromatous plaque. In contrast to STEMI, the thrombus is nonocclusive, but distal vasospasm or embolization may lead to subsequent myocardial necrosis.[7]

It is estimated that MI goes unnoticed or unreported in women in approximately one third of cases as symptoms may be more subtle than in men.[8] Furthermore, there is now a rising population of young women in their third and fourth decades of life who have undetected but significant coronary artery atheroma. Consequently, clinicians working in the office environment need to be alert to the possibility of ACS occurring in women of any age group, particularly when underlying cardiac disease may be exacerbated by anxiety and stress in the perioperative period.


Acute coronary syndrome presents classically with severe central chest pain which is crushing or squeezing in character and may be referred to the left arm or shoulder. There may be associated symptoms of sweating, dyspnea, nausea, or vomiting. In women with ACS, these symptoms may be more prominent than the pain itself. Pain secondary to MI will often last several hours with no respite. In unstable angina, pain usually occurs at rest due to critical myocardial perfusion. This pain will often resolve after 20–30 minutes, either due to spontaneous clot lysis and restoration of a patent coronary artery lumen, or due to relaxation of coronary artery spasm.[7]

Initial management

In the acute setting, it may be difficult for the clinician to differentiate between MI and unstable angina since their clinical presentation may be almost identical. Initial treatment, however, remains the same for both conditions.

Pain in ACS is due to inadequate perfusion and a lack of oxygen delivery to the cardiac muscle. The initial management should therefore aim to maximize the availability of oxygen to the heart and to restore coronary artery patency. High-flow oxygen should be administered via a face mask at 10 L–15 L/minute. The patient should be asked to chew aspirin 300 mg, or to take clopidogrel 300 mg if there is a hypersensitivity to aspirin or major gastrointestinal intolerance.[9, 10]

Sublingual administration of glyceryl trinitrate spray (400 mcg) or administration of an oral nitrate will also help to promote vasodilatation and increase coronary artery perfusion. Nitrates should be avoided if the patient is already hypotensive. The pain of ACS is severe, and intravenous morphine should be titrated to help with this in addition to the administration of an antiemetic.


A 12-lead ECG should be performed as early as possible to look for ST segment elevation, T wave inversion or new left bundle branch block. It should be noted, however, that a normal ECG does not rule out ACS since NSTEMI is more common than STEMI. Cardiac-specific troponins (Troponin I or T) are gold standard diagnostic tests. Troponin level may be normal initially, but usually rises within 2–12 hours and peaks at 12–24 hours post-MI. In an office setting and with a normal ECG, the diagnosis of ACS remains a clinical one, and immediate transfer to a center with percutaneous coronary intervention (PCI) capabilities is indicated, regardless of ECG findings.

Acute asthma


Acute asthma remains a major cause of death among young adults. In the United States there are 5,000–6,000 deaths per year, a good proportion being pre-hospital.

Acute attacks account for 2 million visits to emergency departments every year, with one in 4 leading to admission. Up to one in five inpatients need intensive care with a third of these requiring mechanical ventilation.

Death is most commonly due to asphyxia as a result of a combination of bronchospasm, airway inflammation, and mucous plugging. Other potentially fatal complications include tension pneumothorax, pulmonary edema, pneumonia, and atelectasis.[11]


The patient may give a history of a respiratory tract infection or worsening of previously well-controlled asthma. She may not be able to complete sentences. Although wheeze is common, the severity is not related to the degree of airway compromise: a silent chest indicates almost complete obstruction. The respiratory rate is raised and greater than 25 per minute indicates acute severe asthma, as does a pulse rate greater than 110 bpm. The condition is life threatening when the patient becomes exhausted, has altered level of consciousness, or becomes cyanosed with a silent chest. Arrhythmia and hypotension may intervene.

Initial management

Treatment should be started immediately even if transfer time is short, as patients can become critically ill very rapidly. Initial treatment includes oxygen, inhaled β2 agonists, and steroids. Intravenous access should be obtained. All patients should be given high-flow oxygen, regardless of whether their oxygenation is within the normal range as it may decrease with treatment (see later in the chapter).

Inhaled β2 agonists such as albuteral are potent bronchodilators with a dose-dependent effect and minimal side effects. There is no evidence that nebulizers are more effective than metered dose inhalers; if one method produces no improvement it is sensible to try the alternative. Bronchodilation may result in a decrease in oxygenation due to an increase in ventilation perfusion mismatch. The addition of an anticholinergic agent such as ipratropium bromide has been shown to produce a modest improvement over Inhaled β2 agonists alone.

Because steroids take up to 12 hours to exert their anti-inflammatory effect they should be given early. Dexamethasone 10 mg or methylprednisolone 125 mg should both be given intravenously.

Magnesium sulfate relaxes bronchial smooth muscle and has been shown to be effective in severe acute asthma. The dose is 2 g given over 20 minutes, intravenously.


Any asthmatic patient suffering an attack severe enough to prevent her from finishing sentences, who is tachypnoeic, tachycardic, or showing signs of exhaustion should have continuous pulse oximetry and not be left alone. Baseline spirometry for FEV1 (forced expiratory volume in one second) or peak expiratory flow should be measured and repeated at 30 minute intervals.



Seizures occurring in the office environment are most likely to be secondary to known seizure disorder or a first presentation of epilepsy in a patient. In the United States alone, nearly 2.2 million people suffer from epilepsy; approximately 150,000 new cases of the illness are diagnosed per year.[12]

Although many seizures occur unprovoked, some of the commonest causes of seizures in the absence of primary head trauma include electrolyte disturbance (hypoglycemia is the most common precipitant, particularly in diabetic patients), an intracranial lesion or spontaneous hemorrhage, noncompliance with anti-epileptic medication or sub-therapeutic dosage, stress or anxiety, and use of drugs and/or alcohol.

Iatrogenic causes of seizures which may be directly associated with the performance of certain office gynecological procedures include local anesthetic toxicity and endoscopic fluid resorption leading to water intoxication syndrome.

Initial management

Most seizures are self-terminating, but in some cases a seizure may persist or there may be seizure recurrence. Status epilepticus is defined as a seizure that lasts longer than five minutes or recurrence of seizures without an intervening return of consciousness.[13]

The incidence of permanent brain damage increases with seizure duration.[14] Consequently, in status epilepticus, drug treatment to terminate the seizure state is required as a matter of urgency.

Regardless of the cause of the seizure, the primary goals of treatment in all cases are the same: the protection of the patient’s airway, the prevention of physical injury secondary to convulsions and the rapid termination of the seizure itself. If possible, a patient who is suffering from a seizure should be turned into the left lateral or recovery position to help prevent the aspiration of any regurgitated gastric contents. If the patient is on the operating table, a degree of head-down tilt may also be used to facilitate the drainage of gastric fluid away from the lungs.

High-flow oxygen at 10 L–15 L/minute should be administered via a face mask, vital signs monitored and a patent airway maintained. This can be achieved by simple airway opening maneuvres such as a chin lift or jaw thrust that will prevent the patient’s tongue from falling backward and obstructing the oropharynx. Suction of the oropharynx may be necessary if gastric regurgitation occurs, but this should be performed carefully and under direct vision to avoid causing trauma to friable tissues or a vagal response. In the post-ictal phase, the patient will still need to be monitored closely due to the risk of repeat seizures. Airway opening maneuvres may also still be required at this stage, since airway obstruction can occur secondary to a reduced level of consciousness in the post-ictal state.

If the seizure has not resolved after five minutes, then pharmacologic therapy will be required. First-line drug treatment that can be undertaken in the office environment should be the administration of a benzodiazepine such as lorazepam, diazepam, or midazolam. Intravenous lorazepam (0.1 mg/kg adult dose) is the drug of choice; however, buccal, intramuscular, or rectal benzodiazepines may be quicker to administer in cases where an intravenous cannula is not already in place or where cannulation is difficult. One further dose of the same or a different benzodiazepine should be administered five minutes after the first dose if the seizure is still ongoing.

If no seizure resolution occurs following two doses of benzodiazepine, then the patient will need to be transferred to a definitive care facility for ongoing treatment. The patient is likely to require endotracheal intubation for definitive airway protection prior to transfer, and so urgent and early anesthetic assistance should be sought.


As part of the initial office management of the patient with a seizure, a finger-stick blood glucose should be checked urgently. If this is found to be low (<3 mmol/L or 50 mg/dL), an intravenous infusion of dextrose should be commenced immediately. If there is on site access to a blood gas analyzer, then a venous or arterial blood gas sample may be taken to allow detection and correction of any other abnormal electrolyte levels.



Most procedures undertaken in an office setting are not associated with a high risk of hemorrhage. Occasionally large loop excision of transition zone is associated with significant blood loss. Should there be an undetected coagulopathy (pathological or iatrogenic and undeclared), however, the risk of significant hemorrhage from office procedures is significant.


The patient may complain of an unusual amount of pain for the procedure. Early signs of acute hypovolemia include increased respiratory rate and pulse rate. The patient on beta blockers, however, will not mount a tachycardia. Occasionally there is a paradoxical bradycardia. The patient may complain of feeling faint, dizzy, feeling generally unwell, and/or become agitated or confused. Her skin may become cold and clammy. Capillary refill will be delayed.* Pulse pressure (the difference between systolic and diastolic) may be narrowed: The diastolic is increased. Especially in the pregnant patient, a falling systolic blood pressure is a late sign; it would be a mistake to wait for this sign before initiating treatment.[15]

In pregnancy, the signs of hypovolemia are hidden until a much greater amount of blood is lost from the circulation (see Figure 9-6). Small women have smaller blood volumes and will decompensate earlier.

Figure 9-6

Clinical parameters following increasing blood loss in the pregnant woman.

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