Bronchospasm from hypersensitivity – although extremely rare. Bronchospasm may also be induced in those with a psychogenic element to their illness such as in some asthma sufferers
Relaxation of bronchial musculature
With CNS toxicity:
The higher cortex tends to be excited whereas the mid-brain is depressed
Loss of inhibitory neurones leads to cortical excitability, e.g. fits or tremor
Depression of the mid-brain leads to respiratory collapse.
Non-specific toxicity includes
Methaemoglobinaemia (with prilocaine)
Hypersensitivity reactions:
The preservative methylparaben, used in multidose vials may cause such reactions
Reactions may be local (rash/dermatitis) or generalised
All reactions are unusual; true anaphylaxis is extremely rare and has only been reported in individual case reports. It has been suggested that patients who declare that they are ‘allergic’ should be skin tested, but this should only be considered in those who can describe a clear history of severe reaction. Many cases of ‘allergy’ involving collapse can be attributed to vasovagal faints, and mechanisms not related to hypersensitivity
Intravenous injections
Psychological reactions e.g. anxiety leading to vasovagal collapse
The statistical practice of hypothesis testing is widespread not only in statistics, but also throughout the natural and social sciences. While we are conducting a hypothesis test there a couple of things that could go wrong. There are two kinds of errors, which by design cannot be avoided, and we must be aware that these errors exist. The errors are given the quite pedestrian names of type I and type II errors. What are type I and type II errors, and how we distinguish between them?
Hypothesis Testing
The process of hypothesis testing can seem to be quite varied with a multitude of test statistics. But the general process is the same. Hypothesis testing involves the statement of a null hypothesis, and the selection of a level of significance. The null hypothesis is either true or false, and represents the default claim for a treatment or procedure. For example, when examining the effectiveness of a drug, the null hypothesis would be that the drug has no effect on a disease.
After formulating the null hypothesis and choosing a level of significance, we acquire data through observation. Statistical calculations tell us whether or not we should reject the null hypothesis.
In an ideal world we would always reject the null hypothesis when it is false, and we would not reject the null hypothesis when it is indeed true. But there are two other scenarios that are possible, each of which will result in an error.
Type I Error
The first kind of error that is possible involves the rejection of a null hypothesis that is actually true. This kind of error is called a type I error, and is sometimes called an error of the first kind.
Type I errors are equivalent to false positives. Let’s go back to the example of a drug being used to treat a disease. If we reject the null hypothesis in this situation, then our claim is that the drug does in fact have some effect on a disease. But if the null hypothesis is true, then in reality the drug does not combat the disease at all. The drug is falsely claimed to have a positive effect on a disease.
Type I errors can be controlled. The value of alpha, which is related to the level of significance that we selected has a direct bearing on type I errors. Alpha is the maximum probability that we have a type I error. For a 95% confidence level, the value of alpha is 0.05. This means that there is a 5% probability that we will reject a true null hypothesis. In the long run, one out of every twenty hypothesis tests that we perform at this level will result in a type I error.
Type II Error
The other kind of error that is possible occurs when we do not reject a null hypothesis that is false. This sort of error is called a type II error, and is also referred to as an error of the second kind.
Type II errors are equivalent to false negatives. If we think back again to the scenario in which we are testing a drug, what would a type II error look like? A type II error would occur if we accepted that the drug had no effect on a disease, but in reality it did.
The probability of a type II error is given by the Greek letter beta. This number is related to the power or sensitivity of the hypothesis test, denoted by 1 – beta.
Type II errors can be avoided at the design stage of the study by power calculations that give an indication of how many subjects are required in the trial to minimise the risk of making type 2 error.
How to Avoid Errors
Type I and type II errors are part of the process of hypothesis testing. Although the errors cannot be completely eliminated, we can minimize one type of error.
Typically when we try to decrease the probability one type of error, the probability for the other type increases. We could decrease the value of alpha from 0.05 to 0.01, corresponding to a 99% level of confidence. However, if everything else remains the same, then the probability of a type II error will nearly always increase.
Many times the real world application of our hypothesis test will determine if we are more accepting of type I or type II errors. This will then be used when we design our statistical experiment.
A 72 year old man presents to the emergency department complaining of an itchy rash.
Photo: Dermanet.com
Give 3 possible diagnoses
Give 2 investigations that can be performed in the ED
How would you manage this patient in the ED?
What definitive treatment is required
Answer
Answer
A 72 year old man presents to the department complaining of an itchy rash.
1. Give 3 possible diagnoses
Bullous pemphigoid
Pemphigus
Dermatitis herpetiformis
VZV infection
Bullous erythema multiforme
2. Give 2 investigations that can be performed in the ED
Aspiration of bullous fluid for PCR ? HSV/VZV
Nikolsky’s sign – sliding of skin in pemphagus (not in pemphigoid)
(Definitive diagnosis involves biopsy for histology and immunoflurescence)
3. How would you manage this patient in the ED?
Anlagesia
Anti-histamine for itching
IV Fluids if dehydrated secondary to decreased intake (mucous memb involvement), fluid loss
Dermatology referral
4. What definitive management is required
Dermatology referral for biopsy and steroids/immunosuppression
Exclusion of malignancy in pemphagoid
Few more pictures
Bullous Pemphigoid
Bullous Pemphigoid
Bullous Pemphigoid
Question 2:
A sixty-five year old man has an itchy generalised rash. Your new FY2 doctor thinks the rash is scabies.
Describe the rash. (2 marks)
What is the differential? (2 marks)
Why is this rash itchy? (1 mark)
What is the treatment of choice? (1 mark)
What two features in the history would suggest the diagnosis? (2 marks)
What would you tell the patient? (2 marks)
Answer
Answer
A sixty-five year old man has an itchy generalised rash. Your new SHO thinks the rash is scabies.
1. Describe the rash. (2 marks)
Erythematous papular rash, with excoriations and evidence of burrows.
On the dorsum of the hand
2. What is the differential? (2 marks)
Scabies
Pompholyx
3. Why is this rash itchy? (1 mark)
Allergic/ dermatitic reaction to faeces of scabies mite
4. What is the treatment of choice? (1 mark)
Permethrin, Malathion
What two features in the history would suggest the diagnosis? (2 marks)
Nightime itchy and after hot shower, Genital Itching
f. What would you tell the patient? (2 marks)
Apply at bedtime. Wash off in the morning. Repeat in 1 week.
Treat all household contacts, Launder all bedlinen/clothes/towels
Question 3:
A 45 year old female presents with a wide spread itchy rash and sore mouth.
What is pemphigus?
What is pemhigoid?
How would you differentiate between the two?
How would you manage this patient in the ED?
Answer
Answer
3. A 45 year old female presents with a wide spread itchy rash and sore mouth.
1. What is pemphigus?
Autoimmune disease with deposition of Ig G within epidermis leading to epidermal separation and bullae formation. Commonly begins in middle age, on trunk, face, groin and axillae. Involvement of mucous membranes common, especially oral cavity.
2. What is pemhigoid?
Autoimmune disease with deposition of IgG and C3 on basement membrane with sub-epidermal bullae formation. It is pruritic. Small association with malignancy, increased incidence in 70s. Usually seen on lower limbs especially in inner aspect thigh, then trunk. mucous membrane involvement less than pemphigus vulgaris
3. How would you differentiate between the 2?
Skin biopsy for histology and immunofluorescence.
4. How would you manage this patient in the ED?
Oral or IV analgesia
Anti-histamine to decrease pruritis
IV access and fluids if dehydrated due to oral involvement and fluid loss
Dermatology referral.
Question 4:
An 8 year old boy presents with pain in the wrists, elbow and knee. He has a sore throat 3 weeks ago. Temp 37.8C, other observations normal.
Outline the principles of the Jones criteria in the diagnosis of rheumatic fever (3)
Which four features does this child have (2)
Which other investigation is required? (1)
What are the principles of the treatment of rheumatic fever? (4)
Answer
Answer
An 8 year old boy presents with pain in the wrists, elbow and knee. He has a sore throat 3 weeks ago. Temp 37.8C, other observations normal
1. Outline the principles of the Jones criteria in the diagnosis of rheumatic fever (3)
Diagnosis of rheumatic fever using the Jones criteria requires evidence of recent infection with Group A beta haemolytic streptococci and either 2 major diagnostic criteria or 1 major and 2 minor criteria.
2. Which four features does this child have (2)
Elevated temperature
Prolongation of PR interval
Arthritis of several joints
Erythema marginatum
3. Which other investigation is required? (1)
ASO titre
4. What are the principles of the treatment of rheumatic fever? (4)
Bed rest
Analgesia and anti-pyretic
Aspirin
Use of steroids if evidence of carditis
Penicillin in treatment dose and prophylactically for 5 years if no carditis and life long if carditis
Investigation and treatment of heart valve disease
Splints for arthritis, pain relief
More info
Question 5:
A 22 year old female presents with a painful rash to her legs.
What is the diagnosis?
Give four causes of this rash?
Answer
Answer
A 22 year old female presents with a painful rash to her legs.
1. What is the diagnosis?
Erythema nodosum
2. Give four causes of this rash?
Infective: Tuberculosis, Group A streptococcal throat infections (Scarlet fever, Rheumatic fever), salmonella gastroenteritis, campylobacter colitis, Lymphogranuloma Venereum
Provide a no more than 200 word summary of this paper. Only the first 200 words will be considered and short bullet points are acceptable. [6 marks]
Question 2
Identify 4 weaknesses in the study design. For each one, suggest how that weakness could have been overcome to make the study design more robust. [8 marks]
Question 3
Give 2 examples of how the recruitment process is sub-optimal. [2 marks]
Question 4
The study uses sensitivity/specificity and positive/negative predictive values to depict the performance of high sensitivity troponin. Which performance test from the above is most useful in advising a patient about their chances of having a myocardial infarction? Explain your reasoning. [2 marks]
Question 5
Define sensitivity and specificity. [2 marks]
Question 6
Would the findings in this paper lead you to alter the practice in your ED? Explain your reasoning. [3 marks]
Emergency Departments (EDs) in England provide an essential service for our communities. EDs are under increasing strain as a result of chronic under-resourcing, rising demand, increasing age and acuity of patients, crowding, and higher expectations.
To provide high quality care, EDs need to be properly resourced so that they can meet the demand they face in a safe and effective way.
To drive further improvements in the quality of care, the financial framework should incentivise best practice within EDs, along the same lines that the Best Practice Tariffs operate in other spheres of medical practice.
A paradigm shift is needed. EDs are generally resourced to cope, rather than to deliver safe, high quality care. The accepted image of EDs, reinforced by popular culture, is of fast-paced and even chaotic departments, where rushed staff struggle to cope in the face of adversity. This image, and the underpinning reality, should not be accepted:
EDs see the most critically ill, vulnerable, and risky patients: 24 hours a day, 7 days a week, all year round.
Patients have as much a right to be treated in a calm, orderly environment, by staff with the time to care, as they do, for example, in an operating theatre or intensive care unit.
Staff have a right to offer appropriately paced care to their patients in properly equipped clinical areas, within a workforce that is adequate to deal with the demand faced. The current intensity of ED working, combined with the shift patterns needed to sustain a 24/7 service in the UK, is thought to be behind an emerging crisis in recruitment and retention of staff. This crisis will have a negative impact on patients, and will be more expensive to fix later, than now
The current funding system for Emergency Care is not working:
Tariffs do not accurately or adequately reimburse EDs to provide patients with the care they need. Hospitals are therefore forced to either regard EDs as “loss leaders,” and to fund them in a discretionary way using resources veered from elsewhere in the system, or leave them significantly underfunded.
Tariffs do not incentivise best practice or admission avoidance
Block or managed contracts, where reimbursement for activity is effectively capped, are common
EDs have the ability to function as the powerhouse for effective emergency care by gate-keeping access to hospitals, and by ensuring that patients are diagnosed early, treated correctly from the outset, and sent to the right place for ongoing care. Failure to resource EDs adequately is a waste of a valuable asset. Supporting EDs to do what they should be doing is the only way to deliver round-the-clock, safe, effective, front-loaded care, to our patients. It would also provide true value for money.
There are a few important documents I found in the college and DOH website. Individual links to the pages given below.
Dental infections usually arise from pulpitis and associated necrotic dental pulp that initially begins on the tooth’s surface as dental caries. The infection may remain localised or quickly spread through various fascial planes.
Odontogenic infection may be primary or secondary to periodontal, pericoronal, traumatic, or postsurgical infections. A typical odontogenic infection originates from caries, which decalcify the protective enamel.
Once enamel is dissolved, the infectious caries can travel through the dentinal tubules and gain access to the pulp. In the pulp, the infection may develop a track through the root apex and burrow through the medullar cavity of the mandible or maxilla. The infection then may perforate the cortical plates and drain into the superficial tissues of the oral cavity or track into deeper fascial planes. If the infection does not drain, it will remain localised and develop into a periapical or periodontal abscess.
Serotypes of Streptococcus mutans (cricetus, rattus, ferus, sobrinus) are primarily responsible for causing oral disease.[1] Although lactobacilli are not primary causes, they are progressive agents of caries because of their great acid-producing capacity.
Dental caries is not a life-threatening disease; however, if an odontogenic infection spreads through fascial planes, patients are at risk for sepsis, airway compromise (eg, Ludwig angina, retropharyngeal abscess).
Symptoms and Signs:
Patients with superficial dental infections may complain of localised pain, oedema, and sensitivity to temperature and air. Patients with deep infections or abscesses that spread along the fascial planes may complain of fever and difficulty swallowing, breathing, and opening the mouth.
Local infections
Typically, the tooth is grossly decayed, although it may be normal with cavitated lesions that may have a surrounding chalky demineralised area and swollen erythematous gingiva. Affected teeth generally are tender to percussion and temperature.
Mandibular infections
Submental space infection is characterised by a firm midline swelling beneath the chin and is due to infection from the mandibular incisors.
Sublingual space infection is indicated by swelling of the mouth’s floor with possible tongue elevation, pain, and dysphagia due to anterior mandibular tooth infection.
Submandibular space infection is identified by swelling of the submandibular triangle of the neck around the angle of the jaw. Tenderness to palpation and mild trismus is typical. Infection is caused by mandibular molar infections.
Retropharyngeal space infection is identified by stiff neck, sore throat, dysphagia, hot potato voice, and stridor with possible spread to the mediastinum. These infections are due to infections of the molars.
With spread to the deeper areas of the neck, signs and symptoms of vagal injury, Horner syndrome, and lower cranial nerve injury may be seen.
Infection in this space is more common in children younger than 4 years.
Etiology usually is due to an upper respiratory infection (URI) with spread to retropharyngeal lymph nodes.
Because of high potential for spread to the mediastinum, retropharyngeal space infection is a serious fascial infection.
Ludwig angina (name derived from sensations of choking and suffocation) is characterised by brawny board like swelling from a rapidly spreading cellulitis of the sublingual, submental, and submandibular spaces with elevation and oedema of the tongue, drooling, and airway obstruction.The condition is odontogenic in 90% of cases and arises from the second and third mandibular molars in 75% of cases.
Middle and lateral facial oedema
Buccal space infection is typically indicated by cheek oedema and is due to infection of posterior teeth, usually premolar or molar.
Masticator space infection always presents with trismus manifestation and is due to infection of the third molar of the mandible. Large abscesses may track toward the posterior parapharyngeal spaces. Patients may require fiberoptic nasoendotracheal intubation while awake.
Canine space infection is evidenced by anterior cheek swelling with loss of the nasolabial fold and possible extension to the infraorbital region. This is due to infection of the maxillary canine and potentially may spread to the cavernous sinus.
Gingivitis
Acute narcotising ulcerative gingivitis (Vincent angina, trench mouth) is a condition in which patients present with edematous erythematous gingiva with ulcerated, interdental papillae covered with a gray pseudomembrane.
Patients may have fever and lymphadenopathy and may complain of metallic taste. The condition is caused by invasive fusiform bacteria and spirochetes but is not contagious.
Causative agents:
Serotypes of S mutans are thought to cause initial caries infection. Infections through the fascial planes usually are polymicrobial (average 4-6 organisms). Dominant isolates are anaerobic bacteria.
Anaerobes (75%) – Peptostreptococci, Bacteroides and Prevotella organisms, and Fusobacterium nucleatum
Aerobes (25%) – Alpha-hemolytic streptococci
Investigations:
In dental infection, a FBC count with differential is not mandatory, but a large outpouring of immature granulocytes may indicate the severity of the infection.
Blood cultures in patients who are toxic may help guide management if the course is prolonged.
X-rays to identify involvement of tooth and surrounding bone in the infectious process.
Treatment:
Analgesics and antibiotics may be given if the patient is not systemically ill and appears to have a simple localised odontogenic infection or abscess.
I&D may be required if a periapical or periodontal abscess is identified – Maxfax referral
In deep fascial infections of the neck, an airways assessment might be necessary before the Maxfax referral. If they are systemically unwell, prompt use of IV antibiotics and other measures necessary for a septic patient.
2. Dental Fractures
Types
Clinical Features
ED Treatment
Referral
Infraction
● An incomplete fracture of the enamel without loss of tooth structure.● Not tender. If tenderness is observed evaluate the tooth for a possible luxation injury or a root fracture.
Reassurance
Own dentist
Enamel Fracture
● A complete fracture of the enamel.● Loss of enamel. No visible sign of exposed dentin.
● Not tender. If tenderness is observed evaluate the tooth for a possible luxation or root fracture injury.
● Normal mobility.
ReassuranceDentist treatment
● If the tooth fragment is available, it can be bonded to the tooth.
Own dentist or Emergency Dentist
Enamel-Dentin-Fracture
● A fracture confined to enamel and dentin with loss of tooth structure, but not exposing the pulp.● Percussion test: not tender. If tenderness is observed, evaluate the tooth for possible luxation or root fracture injury.
● Normal mobility.
ReassuranceDentist treatment
● If the tooth fragment is available, it can be bonded to the tooth.
Own Dentist or Emergency Dentist
Enamel-Dentin-Pulp-Fracture
● A fracture involving enamel and dentin with loss of tooth structure and exposure of the pulp.● Normal mobility
● Percussion test: not tender. If tenderness is observed, evaluate for possible luxation or root fracture injury.
● Exposed pulp sensitive to stimuli.
AnalgesiaReassurance
Dentist
Crown Root Fracture without Pulp Exposure
● A fracture involving enamel, dentin and cementum with loss of tooth structure, but not exposing the pulp.● Crown fracture extending below gingival margin.
● Percussion test: Tender.
● Coronal fragment mobile.
● As an emergency treatment a temporary stabilisation of the loose segment to adjacent teeth can be performed until a definitive treatment plan is made.
Dentist or Emergency Dentist
Root Fracture
● The coronal segment may be mobile and may be displaced.● The tooth may be tender to percussion.
● Bleeding from the gingival sulcus may be noted.
● Sensibility testing may give negative results initially, indicating transient or permanent neural damage.
● Reposition, if displaced, the coronal segment of the tooth as soon as possible.
● Check position radiographically.
● Stabilise the tooth with a temporary splint
● Referral to Maxfax or Emergency Dentist
Maxfax or Emergency Dentist
Alveolar Fracture
● The fracture involves the alveolar bone and may extend to adjacent bone.● Segment mobility and dislocation with several teeth moving together are common findings.
● An occlusal change due to misalignment of the fractured
● Reposition any displaced segment and then temporary splint.
Urgent Maxfax referral
Concussion
● The tooth is tender to touch or tapping; it has not been displaced and does not have increased mobility.
Reassurance
Dentist check up
Subluxation
● The tooth is tender to touch or tapping and has increased mobility; it has not been displaced.● Bleeding from gingiva may be noted.
ReassuranceMight need a splint for few weeks through dentist.
Dentist
Extrusive Luxation
● The tooth appears elongated and is excessively mobile.
● Reposition the tooth by gently re-inserting it into the tooth socket.
● Stabilise the tooth for using a temporary splint.
Dentist
Lateral Luxation
● The tooth is displaced, usually in a palatal/lingual or labial direction.● It will be immobile
● Fracture of the alveolar process present.
● Reposition the tooth digitally or with forceps to disengage it from its bony lock and gently reposition it into its original location.● Temporary splint if it is loose.
Maxfax
Intrusive Luxation
● The tooth is displaced axially into the alveolar bone.● It is immobile
● Primary teeth: to allow spontaneous re-eruption except when displaced into the developing successor. Extraction is indicated when the apex is displaced toward the permanent tooth germ.● Permanent teeth: to reposition passively (allowing re-eruption to its preinjury position), actively (repositioning with traction), or surgically and then to stabilise the tooth with a splint for up to 4 weeks in its anatomically correct position
Maxfax / Dentist
Avulsion
● Complete displacement of tooth out of socket.
● Primary teeth: to prevent further injury to the developing successor. Avulsed primary teeth should not be replanted because of the potential for subsequent damage to developing permanent tooth germs.● Permanent teeth: to replant as soon as possible and then to stabilise the replanted tooth in its anatomically correct location to optimise healing of the periodontal ligament and neuromuscular supply while maintaining aesthetic and functional integrity.If replantation of tooth is not possible in the ED, it should be kept in saline, milk or inside of patients mouth moistened by saliva.
INTRODUCTION — Anaphylaxis is a potentially fatal disorder. The rate of occurrence is increasing in industrialised countries. Anaphylaxis is not always recognised as such because it can mimic other conditions and is variable in its presentation.
This topic will review the recognition and treatment of anaphylaxis by healthcare professionals working in emergency department (ED.
DEFINITION AND DIAGNOSIS — Anaphylaxis is defined as a serious allergic or hypersensitivity reaction that is rapid in onset and may cause death. The diagnosis of anaphylaxis is based primarily upon clinical symptoms and signs, as well as a detailed description of the acute episode, including antecedent activities and events occurring within the preceding minutes to hours.
Anaphylaxis is under recognised and undertreated. This may partly be due to failure to appreciate that it can present without obvious skin symptoms and signs and without shock. Anaphylaxis is a much broader syndrome than “anaphylactic shock,” and the goal of therapy should be early recognition and treatment with adrenaline to prevent progression to life-threatening respiratory and/or cardiovascular symptoms and signs, including shock.
Diagnostic criteria — Diagnostic criteria for anaphylaxis were published by a multidisciplinary group of experts in 2005 and 2006. These criteria were intended to help clinicians recognise the full spectrum of symptoms and signs that comprise anaphylaxis.
There are three diagnostic criteria, each reflecting a different clinical presentation of anaphylaxis. Anaphylaxis is highly likely when any ONE of the following three criteria is fulfilled:
Criterion 1 — Acute onset of an illness (minutes to several hours) involving the skin, mucosal tissue, or both (eg, generalized hives, pruritus or flushing, swollen lips-tongue-uvula) and at least one of the following:
Reduced blood pressure (BP) or associated symptoms and signs of end-organ dysfunction (eg, hypotonia [collapse] syncope, incontinence). (See ‘Criterion 3′ below.)
Note: Skin symptoms and signs are present in up to 90 percent of anaphylactic episodes. This criterion will therefore frequently be helpful in making the diagnosis.
Criterion 2 — Two or more of the following that occur rapidly after exposure to a LIKELY allergen for that patient (minutes to several hours):
Involvement of the skin-mucosal tissue (eg, generalized hives, itch-flush, swollen lips-tongue-uvula).
Reduced BP or associated symptoms and signs (eg, hypotonia [collapse], syncope, incontinence).
Persistent gastrointestinal symptoms and signs (eg, crampy abdominal pain, vomiting).
Note: Skin symptoms or signs are absent or unrecognised in up to 20 percent of anaphylactic episodes. Criterion 2 incorporates symptoms and signs in other organ systems and is applied to patients with exposure to a substance that is a likely allergen for them.
Criterion 3 — Reduced BP after exposure to a KNOWN allergen for that patient (minutes to several hours):
Reduced BP in adults is defined as a systolic BP of less than 90 mmHg or greater than 30 percent decrease from that person’s baseline
In infants and children, reduced BP is defined as low systolic BP (age specific)* or greater than 30 percent decrease in systolic BP
Note: Criterion 3 is intended to detect anaphylactic episodes in which only one organ system is involved and is applied to patients who have been exposed to a substance to which they are known to be allergic, for example, hypotension or shock after an insect sting.
There will occasionally be patients who do not fulfill any of these criteria, but for whom the administration of adrenaline is appropriate. As an example, it would be appropriate to administer adrenaline to a patient with a history of near-fatal anaphylaxis to peanut who presents with urticaria and flushing that developed within minutes of a known unintentional ingestion of peanut.
Symptoms and signs— Anaphylaxis may present with various combinations of approximately 40 potential symptoms and signs.
Common symptoms and signs of anaphylaxis include the following:
Skin symptoms and signs, which occur in up to 90 percent of episodes, including generalized hives, itching or flushing, swollen lips-tongue-uvula, periorbital edema, conjunctival swelling.
Respiratory symptoms and signs, which occur in up to 70 percent of episodes, including nasal discharge, nasal congestion, change in voice quality, sensation of throat closure or choking, stridor, shortness of breath, wheeze, cough.
Gastrointestinal symptoms and signs, which occur in up to 45 percent of episodes, including nausea, vomiting, diarrhea, and crampy abdominal pain.
Cardiovascular symptoms and signs, which occur in up to 45 percent of episodes, including hypotonia (collapse), syncope, incontinence, dizziness, tachycardia, and hypotension.
The factors that determine the course of anaphylaxis in an individual patient are not fully understood. At the onset of an anaphylactic episode, it is not possible to predict how severe it will become, how rapidly it will progress, and whether it will resolve promptly and completely or become biphasic or protracted.
Death from anaphylaxis usually results from asphyxiation due to upper airway edema or respiratory failure due to bronchial obstruction, and less commonly, from cardiovascular collapse.
Time course — Anaphylaxis is usually characterized by a defined exposure to a potential trigger, followed by rapid onset, evolution, and resolution of symptoms and signs within minutes to hours.
TRIGGERS — Most anaphylaxis episodes are triggered through an immunologic mechanism involving IgE. Foods are the most common trigger in children, while medications and insect stings are more common triggers in adults than in children.
CONTRIBUTORY FACTORS — Comorbidities and concurrent medications may impact the severity of symptoms and signs and response to treatment in patients with anaphylaxis.
Comorbidities — Asthma and cardiovascular disease are the most important risk factors for a poor outcome from anaphylaxis. Other disorders may also increase risk.
Persistent asthma is a risk factor for anaphylaxis. Asthma is also associated with increased risk of death from anaphylaxis, especially in adolescents and young adults with poorly controlled disease.
Cardiovascular disease is an important risk factor for death from anaphylaxis in middle-aged and older individuals.
Other respiratory diseases, eg, chronic obstructive pulmonary disease (COPD), interstitial lung disease, or pneumonia are also risk factors for severe or fatal anaphylaxis in older adults.
Concurrent medications — Concurrent administration of certain medications, such as beta-adrenergic blockers, angiotensin-converting enzyme inhibitors, and alpha-adrenergic blockers may increase the likelihood of severe or fatal anaphylaxis, and may also interfere with the patient’s ability to respond to treatment and with the patient’s compensatory physiologic responses.
Beta-adrenergic blockers, administered orally, parenterally, or topically (eg, eye drops) are sometimes associated with severe anaphylaxis and may also potentially make anaphylaxis more difficult to treat by causing unopposed alpha-adrenergic effects. They also can worsen hypotension, as well as reduce the bronchodilator and cardiovascular response to the beta-adrenergic effects of endogenous or exogenous adrenaline.
Alpha-adrenergic blockers may decrease the effects of endogenous or exogenous adrenaline at alpha-adrenergic receptors, potentially making anaphylaxis less responsive to the alpha-adrenergic effects of adrenaline.
ACE inhibitors are of particular importance in regards to patients who have experienced anaphylaxis to Hymenoptera venom.
LABORATORY TESTS — The clinical diagnosis of anaphylaxis can sometimes be supported by documentation of elevated concentrations of serum or plasma total tryptase or plasma histamine. It is critical to obtain blood samples for measurement of these mast cell and basophil mediators soon after the onset of symptoms, because elevations are transient.
Serum or plasma total tryptase – The standardized assay for measurement of total serum or plasma tryptase is widely available in clinical laboratories (normal range 1 to 11.4 ng/mL, Phadia AB, Uppsala, Sweden). In infants under age six months, normal baseline total tryptase concentrations are higher than they are in older infants, children, and adults. Optimally, the blood sample for tryptase measurement needs to be obtained from 15 minutes to 3 hours of symptom onset. A tryptase level that is within normal limits cannot be used to refute the clinical diagnosis of anaphylaxis.
Serial measurements of total tryptase in serum or plasma over several hours may increase the sensitivity and the specificity of the tests.
Plasma histamine – Plasma histamine levels typically peak within 5 to 15 minutes of the onset of anaphylaxis symptoms, and then decline to baseline by 60 minutes due to rapid metabolism by N-methyltransferase and diamine oxidase. Elevated plasma histamine levels correlate with anaphylaxis symptoms and signs, and are more likely to be increased than are total serum tryptase levels.
DIFFERENTIAL DIAGNOSIS — Approximately 40 other diseases and conditions might need to be considered in the differential diagnosis of anaphylaxis. The most common disorders in the differential diagnosis include acute generalized urticaria and/or angioedema, acute asthma exacerbations, syncope/faint, and anxiety/panic attacks
IMMEDIATE MANAGEMENT — Prompt assessment and treatment are critical in anaphylaxis, as respiratory or cardiac arrest and death can occur within minutes. The cornerstones of initial management are the following:
Removal of the inciting antigen, if possible (eg, stop infusion of a suspect medication)
Call for help (summon a resuscitation team in a hospital setting, or call 999 or an equivalent emergency medical services number in a community setting)
Intramuscular injection of adrenaline. IM into the mid-outer aspect of the thigh.
Placement of the patient in the supine position with the lower extremities elevated, or if dyspneic or vomiting, placement of the patient semi-recumbent with lower extremities elevated
Supplemental oxygen (8-10 liters by face mask)
Volume resuscitation with intravenous fluids
Two large-bore intravenous catheters (ideally 14 to 16 gauges for most adults) should be inserted in preparation for rapid administration of fluids and medications.
In normotensive adults, isotonic (0.9 percent) saline should be infused at a rate of 125 mL per hour to maintain venous access.
Continuous electronic monitoring of cardiopulmonary status, including blood pressure, heart rate, and respiratory rate, and monitoring of oxygen saturation by pulse oximetry is required for the duration of the episode.
Intubation should be performed immediately if marked stridor or respiratory arrest is present.
Intravenous fluids — Intravenous access should be obtained in case fluid resuscitation is required. Massive fluid shifts can occur rapidly in anaphylaxis due to increased vascular permeability, with transfer of up to 35 percent of the intravascular volume into the extravascular space within minutes.
The following principles should guide therapy:
Fluid resuscitation should be initiated immediately in patients who present with orthostasis, hypotension, or incomplete response to intramuscular adrenaline.
Adults should receive 1 to 2 liters of normal saline at a rate of 5 to 10 mL/per kilogram in the first minutes of treatment. Large volumes of fluid (eg, up to 7 liters) may be required.
Children should receive normal saline in boluses of 20 mL per kilogram, each over 5 to 10 minutes, and repeated as needed. Large volumes of fluid (up to 100 mL per kilogram) may be required.
Normal saline is preferred over other solutions in most situations, because other solutions have potential disadvantages:
Lactated Ringer’s solution can potentially contribute to metabolic acidosis
Dextrose is rapidly extravasated from the circulation into the interstitial tissues
Colloid solutions (eg, albumin or hydroxyethyl starch) confer no survival advantage in patients with distributive shock and are more costly [71]
PHARMACOLOGIC TREATMENTS —
Adrenaline — Adrenaline is the drug of choice for anaphylaxis. The pharmacologic actions of this agent address the pathophysiologic changes that occur in anaphylaxis better than any other medication. It decreases mediator release from mast cells. Moreover, it is the only medication that prevents or reverses obstruction to airflow in the upper and lower respiratory tracts, and prevents or reverses cardiovascular collapse.
Therapeutic actions and adverse effects — The therapeutic actions of adrenaline include the following:
Alpha-1 adrenergic agonist effects: increased vasoconstriction, increased peripheral vascular resistance, and decreased mucosal edema (eg, in the upper airway).
Beta-1 adrenergic agonist effects: increased inotropy and increased chronotropy.
Beta-2 adrenergic agonist effects: increased bronchodilation and decreased release of mediators of inflammation from mast cells and basophils.
Dosing and administration —
Intramuscular injection — Intramuscular injection is recommended over subcutaneous injection because it consistently provides a more rapid increase in the plasma and tissue concentrations of adrenaline. The adrenaline dilution for intramuscular injection contains 1 mg per mL and may also be labeled as 1:1000.
For adults, the recommended dose of adrenaline (1 mg per mL) is 0.3 to 0.5 mg per single dose, injected intramuscularly into the mid-outer thigh (vastus lateralis muscle). Based on clinical experience and consensus opinion, this dose may be repeated at 5 to 15 minute intervals. Typically, only one or two additional doses are needed.
For infants and children, the recommended dose of adrenaline (1 mg per mL) is 0.01 mg per kilogram (up to 0.5 mg per dose in a child weighing 50 kg or more), injected intramuscularly into the mid-outer thigh (vastus lateralis muscle). The dose should be drawn up using a 1 mL syringe. This treatment may be repeated at 5 to 15 minute intervals.
Intravenous infusion and indications — Patients who do not respond to intramuscular injection of adrenaline and fluid resuscitation may not be adequately perfusing muscle tissues, as most commonly occurs in individuals presenting with profound hypotension or symptoms and signs suggestive of impending shock (dizziness, incontinence of urine and/or stool). Such patients should receive adrenaline by SLOW intravenous infusion, with the rate titrated according to response and the presence of continuous hemodynamic monitoring.
The adrenaline dilution for intravenous infusion contains 0.1 mg/mL and may also be labeled 1:10,000.
For adults, the initial dose for intravenous adrenaline infusion is 2 to 10 micrograms per minute, titrated to effect on blood pressure with continuous noninvasive monitoring.
For infants and children, the dose for intravenous infusion of adrenaline is 0.1 to 1 microgram per kilogram per minute, titrated to effect on blood pressure with continuous noninvasive monitoring.
Situations requiring caution — There are NO absolute contraindications to adrenaline use in anaphylaxis.
Subgroups of patients might theoretically be at higher risk for adverse effects during adrenaline therapy. Formal risk-benefit analyses are not possible.
Patients with cardiovascular diseases: reluctance to administer adrenaline due to fear of adverse cardiac effects should be countered by the awareness that the heart is a target organ in anaphylaxis. In the healthy human heart, mast cells are present throughout the myocardium and in the intima of coronary arteries. In patients with coronary artery disease, mast cells are found in atherosclerotic lesions and contribute to atherogenesis. Anaphylaxis can unmask subclinical coronary artery disease, and myocardial infarction and/or arrhythmias can occur during anaphylaxis, even if adrenaline is not injected. Moreover, anaphylaxis itself can cause vasospasm, arrhythmias, and myocardial infarction in patients, including children, with healthy hearts as confirmed by normal electrocardiograms, echocardiography, and other studies after resolution of anaphylaxis.
Patients receiving monoamine oxidase inhibitors (which block adrenaline metabolism), or tricyclic antidepressants (which prolong adrenaline duration of action).
Patients with certain preexisting conditions, such as recent intracranial surgery, aortic aneurysm, uncontrolled hyperthyroidism or hypertension, or other conditions that might place them at higher risk for adverse effects related to adrenaline.
Patients receiving stimulant medications (eg, amphetamines or methylphenidate used in the treatment of attention deficit hyperactivity disorder) or abusing cocaine that might place them at higher risk for adverse effects from adrenaline.
Adjunctive agents — Adjunctive therapies for the treatment of anaphylaxis include antihistamines, bronchodilators, glucocorticoids, and other vasopressors in addition to adrenaline.
H1 antihistamines —
H1 antihistamines relieve itch and hives. These medications DO NOT relieve upper or lower airway obstruction, hypotension or shock, and in standard doses do not inhibit mediator release from mast cells and basophils. For parenteral treatment, only first-generation agents are available:
H2 antihistamines — There is minimal evidence to support the use of H2 antihistamines in conjunction with H1 antihistamines in the emergency treatment of anaphylaxis.
If used, ranitidine (50 mg in adults) (12.5 to 50 mg [1 mg per kilogram] in children), may be diluted in 5 percent dextrose to a total volume of 20 mL and injected intravenously over five minutes.
Bronchodilators — For the treatment of bronchospasm not responsive to adrenaline, inhaled bronchodilators, such as salbutamol should be administered by nebulizer/compressor as needed.
Glucocorticoids — The onset of action of glucocorticoids takes several hours; therefore, these medications do not relieve the initial symptoms and signs of anaphylaxis. The rationale for giving them is to prevent the biphasic or protracted reactions.
CARE UPON RESOLUTION — To reduce the risk of recurrence, patients who have been successfully treated for anaphylaxis subsequently require confirmation of the anaphylaxis trigger, as well as anaphylaxis education.
Observation — There is no consensus regarding the optimal observation period for a patient who has been successfully treated for anaphylaxis in a healthcare facility. The following are suggested:
Patients with moderate anaphylaxis who do not respond promptly to adrenaline, and all patients with severe anaphylaxis, should be admitted to an observation unit or to a hospital.
For patients with anaphylaxis that resolved promptly and completely with treatment, we suggest a minimum observation period of a few hours, and prefer a period of 8 to 10 hours, if possible. We also suggest that if patients are sent home after only a few hours, they should be trained to use an adrenaline autoinjector.
SUMMARY AND RECOMMENDATIONS
Anaphylaxis is a serious allergic reaction that is rapid in onset and may cause death.
There are three clinical criteria for the diagnosis of anaphylaxis, which reflect the different ways in which anaphylaxis may present.
Recognition is not always easy, because anaphylaxis can mimic many other disorders and can be variable in its presentation.
Patients and healthcare professionals commonly fail to recognize and diagnose anaphylaxis in its early stages, when it is most responsive to treatment.
Anaphylaxis most often results from an IgE-mediated allergic reaction. Common triggers include foods, insect stings, and medications.
The clinical diagnosis of anaphylaxis may or may not be confirmed by measurement of elevated concentrations of plasma histamine or serum or plasma total tryptase. Elevations in these mediators are transient. Serum tryptase is seldom elevated in food-triggered anaphylaxis or in normotensive patients with anaphylaxis.
Prompt recognition and treatment are critical in anaphylaxis. In fatal anaphylaxis, median times to cardiorespiratory arrest are 5 minutes in iatrogenic anaphylaxis, 15 minutes in stinging insect venom-induced anaphylaxis, and 30 minutes in food-induced anaphylaxis.
Adrenaline is lifesaving in anaphylaxis. It should be injected as early as possible in the episode in order to prevent progression of symptoms and signs. There are no absolute contraindications to adrenaline use, and it is the treatment of choice for anaphylaxis of any severity.
For adults, the dose of adrenaline is 0.3 mg to 0.5 mg, injected intramuscularly into the mid-outer thigh. This treatment may be repeated at 5 to 15 minute intervals.
For infants and children, the dose of adrenaline is 0.01 mg per kilogram up to 0.5 mg per dose, injected intramuscularly into the mid-outer thigh. This treatment may be repeated at 5 to 15 minute intervals.
Massive fluid shifts can occur in anaphylaxis, and all patients with orthostasis, hypotension, or incomplete response to adrenaline should receive large volume fluid resuscitation with normal saline.
Food is a particularly common trigger in children, while medicinal products are much more common triggers in older people.
One in 1333 of the population of England has experienced anaphylaxis at some point in their lives
Approximately 20 deaths from anaphylaxis reported each year in the UK
Document the acute clinical features (airway, breathing, circulation, associated skin and mucosal symptoms)
Record the time of onset of the reaction
Record possible trigger factor.
Take blood sample for mast cell tryptase (1st sample straight after receiving emergency treatment and 2nd sample after 1-2 hrs after starting the symptoms)
Adult and young people (16, 17yrs) should observe for 6-12 hrs from the onset of symptoms depending on the response to treatment.
Paediatric patient need to be admitted for longer observation.
At discharge all suspected anaphylaxis patient should have 1) referral to allergy services, 2) adrenaline injector and 3) patient information on anaphylaxis.
Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) refer to the sudden cessation of cardiac activity with hemodynamic collapse, typically due to sustained ventricular tachycardia/ventricular fibrillation. These events mostly occur in patients with structural heart disease (that may not have been previously diagnosed), particularly coronary heart disease.
SCA most commonly results from hemodynamic collapse due to ventricular fibrillation (VF) in the setting of structural heart disease.
The outcome following SCA depends upon numerous factors including the underlying cause and the rapidity of resuscitation.
Most individuals suffering from SCA become unconscious within seconds to minutes as a result of insufficient cerebral blood flow. There are usually no premonitory symptoms. If symptoms are present, they are nonspecific and include chest discomfort, palpitations, shortness of breath, and weakness.
DEFINITIONS — Various criteria have been used to define SCA and SCD in the medical literature.
The following definitions of SCA and SCD were presented by American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) in 2006:
“[Sudden] cardiac arrest is the sudden cessation of cardiac activity so that the victim becomes unresponsive, with no normal breathing and no signs of circulation. If corrective measures are not taken rapidly, this condition progresses to sudden death. Cardiac arrest should be used to signify an event as described above, that is reversed, usually by CPR and/or defibrillation or cardioversion, or cardiac pacing. Sudden cardiac death should not be used to describe events that are not fatal.”
EPIDEMIOLOGY — The risk of experiencing SCA is increased by a number of factors. The incidence increases dramatically with age and with underlying cardiac disease. In addition, men are two to three times more likely to experience SCA than women.
The magnitude of the influence of underlying cardiac disease on the risk of SCA is illustrated by the following observations:
The risk of SCA is increased six- to ten-fold in the presence of clinically recognised heart disease, and two- to four-fold in the presence of coronary heart disease (CHD) risk factors.
SCD is the mechanism of death in over 60 percent of patients with known CHD.
ETIOLOGY — SCA usually occurs in people with some form of underlying structural heart disease, most notably CHD. Coronary heart disease — As much as 70 percent of SCAs have been attributed to CHD. Among patients with CHD, SCA can occur both during an acute coronary syndrome (ACS) and in the setting of chronic, otherwise stable CHD.
Other structural heart disease — Other forms of structural heart disease, both acquired and hereditary, account for approximately 10 percent of cases of out-of-hospital SCA. Examples of such disorders include the following:
Heart failure and cardiomyopathy in which SCD is responsible for approximately one-third of deaths.
Left ventricular hypertrophy due to hypertension or other causes.
Myocarditis.
Hypertrophic cardiomyopathy.
Arrhythmogenic right ventricular cardiomyopathy.
Congenital coronary artery anomalies.
Mitral valve prolapse.
Absence of structural heart disease — In different reports, approximately 10 to 12 percent of cases of SCA among subjects under age 45 occur in the absence of structural heart disease.
This can occur in a variety of settings:
Brugada syndrome.
Idiopathic VF, also called primary electrical disease.
Congenital or acquired long QT syndrome
Arrhythmogenic right ventricular cardiomyopathy.
Familial polymorphic ventricular tachycardia, also called “catecholaminergic polymorphic VT”.
Familial SCD of uncertain cause.
Wolff-Parkinson-White syndrome.
Acute triggers — In addition to the presence of the above underlying disorders, superimposed triggers for SCA appear to play a major role in the pathogenesis of this disorder. These include ischemia, electrolyte disturbances (particularly hypokalemia and hypomagnesemia), the proarrhythmic effect of some antiarrhythmic drugs, autonomic nervous system activation, and psychosocial factors.
RISK FACTORS — A number of clinical characteristics and other factors are associated with an increased risk of SCA among persons without prior clinically recognized heart disease. Most risk factors for CHD are also risk factors for SCA.
Cigarette smoking — Current cigarette smoking and the number of cigarettes smoked per day among current smokers are strongly related to the risk of SCA in patients with CHD.
Exercise — The risk of SCA is transiently increased during and up to 30 minutes after strenuous exercise compared to other
Regular exercise is associated with a lower resting heart rate and increased heart rate variability, characteristics associated with a reduced risk of SCA
Family history of SCA — A family history of SCA, either alone or with myocardial infarction, is associated with a 1.5 to 1.8-fold increased risk of
Serum CRP — Chronic inflammation, as manifested in part by higher serum concentrations of C-reactive protein (CRP), has been implicated as a risk factor for a variety of cardiovascular diseases (including acute coronary syndromes, stroke, and the efficacy of lipid lowering with statins). Elevated serum CRP is also associated with an increased risk of SCA
Excess alcohol intake — Moderate alcohol intake (eg, one to two drinks per day, and avoidance of binge drinking) may decrease the risk of SCD. In comparison, heavy alcohol consumption (six or more drinks per day) or binge drinking increases the risk for SCD
Psychosocial factors — Clinical observations have suggested a possible relation between acutely stressful situations and the risk of SCA
Fatty acids — Elevated plasma nonesterified fatty acid (free fatty acid) concentrations are associated with ventricular arrhythmias and SCD after a myocardial infarction and, after adjustment for confounding factors, in the general.
MANAGEMENT — The acute management of cardiac arrest is according to ALS Guidelines.
Management of cardiopulmonary arrest in pregnancy
Cardiopulmonary arrest during pregnancy presents a unique clinical scenario involving two patients: the mother and the foetus. Management of these patients demands a rapid multidisciplinary approach, including anesthesiology, medicine, obstetrics, neonatology and sometimes cardiothoracic surgery. Basic and advanced cardiac life support algorithms should be implemented; however, the physiological and anatomical changes of pregnancy require some modifications to these protocols.
This topic will focus on management of cardiopulmonary arrest during pregnancy.
PREVALENCE OF CARDIAC ARREST IN PREGNANCY — The prevalence of cardiac arrest in pregnant women varies from 1/20,000 to 1/50,000 ongoing pregnancies. The increasing prevalence and severity of maternal obesity, rising cesarean delivery rates, and advances in reproductive options for women with chronic illnesses and at older ages have elevated the medical acuity level of obstetrical practice and may be elevating the frequency of cardiac arrest in pregnant women.
AETIOLOGY — Cardiac arrest may be related to conditions unique to pregnancy or etiologies found in the nongravid state. In one review, the most common causes in pregnant women in the United States and United Kingdom were:
Pulmonary embolism (29 percent),
Haemorrhage (17 percent),
Sepsis (13 percent),
Peripartum cardiomyopathy (8 percent),
Stroke (5 percent),
Preeclampsia-eclampsia (2.8 percent),
Complications related to anesthesia (eg, difficult or failed intubation, local anesthetic toxicity, aspiration) (2 percent),
Reversible causes of cardiac arrest should be treated promptly (eg, electrolyte abnormalities, tamponade, hypothermia, hypovolemia, hypoxia, hypomagnesemia, myocardial infarction, poisoning, pulmonary embolism, tension pneumothorax).
RESUSCITATION DURING PREGNANCY — Resuscitation of the pregnant women involves:
In the USA they call for “maternal code blue”, but in the UK, usual cardiac arrest call (2222) and Gynae/Obs registrar fast bleep (Correct me if I am wrong.)
If the uterus is above the umbilicus, displace the uterus laterally and to the left (ie, left uterine displacement)
Initiate the ABCs using pregnancy modifications
Estimate the gestational age of the fetus (See ‘Determining gestational age’ below.)
If the uterine fundus is ≥4 fingerbreadths above the umbilicus, at four minutes, begin perimortem cesarean delivery and complete delivery by five minutes following cardiac arrest
At 15 minutes, if resuscitation remains unsuccessful, initiate direct cardiac massage if appropriate resources and personnel are available. Thoracotomy and open chest message would be particularly effective for patients with chest trauma, tension pneumothorax, massive pulmonary embolism, pericardial tamponade, and in patients with chest or spine deformities.
Ongoing interventions: evaluate need to institute cardiopulmonary bypass therapy.
Continue resuscitation measures until all resources and attempts have been exhausted. This will vary depending upon the clinical circumstances and resources of the facility.
ABCs — The ABCs (airway, breathing, circulation) of resuscitation are well-described.
In pregnant women with uterine fundal height at or beyond the umbilicus, the uterus should be displaced to the patient’s left to minimize aortocaval compression.
Active airway management is the initial consideration. Pregnant women are at increased risk of rapidly developing hypoxemia because of decreased functional residual capacity and increased oxygen consumption. Both intubation and bag mask ventilation can be more difficult in the late stages of pregnancy and back-up airway procedures, including cricothyrotomy, may be required in some cases. The increased risk of aspiration and narrowing of upper airways, particularly in the third trimester, require special consideration during pregnancy. Intubation via direct or video laryngoscopy using cricoid pressure and 100 percent oxygen is performed using a smaller sized endotracheal tube (0.5 mm to 1.0 mm less in internal diameter compared to that used for nonpregnant women). Endotracheal tube placement should be verified using capnography or an esophageal detector device.
For chest compressions, hand placement should be more cephalad than in nonpregnant women to accommodate the upward displacement of the diaphragm by the gravid uterus. Although specific landmarks have not been established, it is suggested that performing chest compressions slightly above the center of the sternum to adjust for the elevation of the diaphragm associated with the gravid uterus.
Intravenous access should be established above the groin area since drugs administered via the femoral vein may not reach the maternal heart until the fetus is delivered. Access to an antecubital vein with two 14-gauge catheters can be as effective as central line catheters for volume replacement, but do not allow hemodynamic monitoring.
Avoiding aortocaval compression — Supine positioning optimises the vectors required for effective chest compressions in the nonpregnant patient; however, left lateral uterine displacement is necessary in the pregnant patient with fundal height at, or above, the umbilicus, to minimise aortocaval compression (supine hypotensive syndrome), optimise venous return, and generate cardiac output during CPR.
Methods to achieve left lateral uterine displacement include:
Manual uterine displacement
Tilt of the operating room table, or
Placement of pillows, a wood or foam resuscitation wedge (eg, Cardiff wedge) or rolled up towels or blankets
If a suitable wedge is not available, the patient can be tilted upon a rescuer (the rescuer sits on his/her heels and uses his/her thighs as a wedge under the patient). Manual uterine displacement is preferred since it preserves the supine positioning of the upper torso for optimal chest compression vector forces. A hand is used to apply maximal leftward push to the right upper border of the uterus to achieve a displacement of about 1.5 inches from the midline.
Defibrillation — Management of ventricular arrhythmias may require defibrillation during maternal resuscitation. The physiological changes of pregnancy, including increases in blood volume and decreases in functional residual capacity, do not appear to alter transthoracic impedance or transmyocardial current. Therefore, current energy requirements for adult defibrillation are appropriate for use in pregnant women.
Determining gestational age — In pregnant women, determining gestational age is critical, as the likelihood of neonatal viability is a factor in decision-making. If the prenatal record is not available, physical examination can aid in establishing the gestational age. Uterine size correlates with gestational age, but can be misleading in some situations, such as when there is a multiple gestation, large fibroids, or severe oligohydramnios or polyhydramnios. The formula for estimating gestational age by physical examination is: distance from the top of the symphysis pubis to the top of the fundus (cm) = gestational age (weeks).
Foetal monitoring — In general, the status of the mother should guide management during the resuscitation process; if the status of the mother is poor and deteriorating, the status of the foetus will be further compromised. Therefore, foetal monitoring is not recommended during the resuscitation process.
Delivery as part of the resuscitation process — Despite implementation of maneuvers to ameliorate aortocaval compression, CPR may not restore spontaneous circulation or provide adequate cardiac output. Blood flow during CPR is produced by mechanical compression of the heart between the sternum and the spine and phasic fluctuations in intrathoracic pressure. Despite appropriate use of leftward uterine displacement, the mechanical effects of the gravid uterus can decrease venous return from the inferior vena cava, obstruct blood flow through the abdominal aorta, and diminish thoracic compliance, all of which contribute to unsuccessful CPR. Without restoration of cardiac output, both mother and fetus are at risk for hypoxia and eventually anoxia, especially when interruption of normal cardiac and respiratory function persists beyond four minutes. Although it may be counterintuitive to operate on a haemodynamically unstable patient, cesarean delivery may be life-saving for both mother and fetus in this situation. Delivery of the baby empties the uterus, relieving the aortocaval compression. This results in a 60 to 80 percent increase in cardiac output, thereby increasing the likelihood of maternal survival.
The American Heart Association recommends cesarean delivery if maternal resuscitative efforts have not been successful within four minutes. The rationale for this approach is that:
Irreversible brain damage can occur in nonpregnant individuals after four to six minutes of anoxia
Pregnant women become anoxic sooner than nonpregnant women because of decreased functional residual capacity
If the uterine fundus is ≥4 fingerbreadths above the umbilicus, ineffective resuscitation efforts may become effective when the uterus is no longer gravid and potentially causing aortocaval compression
Intact fetal survival diminishes as the time between maternal death and delivery lengthens
“Five minute rule” — Although there have been no controlled clinical trials in this area, a review of case reports of perimortem cesarean delivery from 1900 to 1985 suggested that normal neonatal neurological outcome was most likely when delivery occurred within five minutes of maternal cardiac arrest. In this series, 42 of 42 infants delivered within five minutes had a normal neurological outcome compared with 7 of 8 infants delivered within 6 to 10 minutes, 6 of 7 infants delivered within 11 to 15 minutes, 0 of 1 infant delivered between 16 and 20 minutes, and 1 of 3 infants delivered within 21 to 25 minutes.
Minimum gestational age — The minimum gestational age for perimortem cesarean delivery is controversial. Although physiologically aortocaval compression begins as early as 20 weeks, there is some imprecision within the range of 20 to 24 weeks. Neonatal viability is also an imprecise assessment, as it is uncertain which extremely preterm infants, particularly those born at 23 and 24 weeks of gestation, have a reasonable chance of survival without severe deficits. Most centers would provide full neonatal support to infants at least 24 weeks of gestation and some centers provide this level of care to infants greater than 22 weeks of gestation.
Delivery issues — As discussed above, perimortem cesarean should be performed within five minutes after cardiac arrest, thus transporting the patient to an operating room is not a priority. An emergency cesarean delivery kit should be part of the resuscitation cart in patient care areas that commonly serve pregnant women or transported to the location of the pregnant patient who has arrested.
Chest compressions should be continued without interruption until return of spontaneous circulation and broad spectrum antibiotics should be administered to decrease the risk of postpartum infection.
We suggest a vertical skin incision to provide fast entry, adequate uterine exposure, and access to the diaphragm, which may be useful for further resuscitative interventions. Bleeding may be minimal during the procedure due to hypoperfusion. Extraction of the placenta and closure of the hysterotomy are important steps to prevent subsequent hemorrhage when hemodynamic stability is eventually restored.
Medications use for CPR during pregnancy — Given the lethality of cardiopulmonary arrest, the benefits from use of potentially life-saving drugs outweigh any known or possible feral risks. All medications for treatment of cardiopulmonary arrest in the nonpregnant patient are used for the pregnant patient.
If magnesium toxicity (following treatment of pre-eclempsia/eclempsia) is suspected, magnesium sulfate infusion should be discontinued and calcium gluconate (10 mL of a 10 percent solution)
Sodium bicarbonate is not routinely given during CPR, but it may be useful in life-threatening hyperkalemia or tricyclic antidepressant overdose.
Arryhthmias are difficult to control, especially those resulting from bupivacaine toxicity. Amiodarone is the favored treatment for severe bupivacaine-induced arrhythmias. Early administration of lipid emulsion (eg, 20 percent intralipid) is becoming a significant component in resuscitation of bupivacaine-induced cardiotoxicity.
ADDITIONAL INTERVENTIONS — After 15 minutes of unsuccessful closed chest CPR, direct cardiac massage via thoracotomy or through the diaphragm (if the abdomen is open) can be implemented. Direct cardiac massage results in near normal systemic perfusion throughout the compression cycle and with higher cranial and myocardial flow than achieved with external chest compressions of conventional CPR.
For pregnant women with ST elevation myocardial infarction, percutaneous coronary intervention is the preferred reperfusion strategy since fibrinolytics are relatively contraindicated in pregnancy.
Successful fibrinolysis has been reported for massive pulmonary embolism and for ischemic stroke during pregnancy.
MATERNAL OUTCOME — A multicenter study reported outcomes of 55 women with a cardiac arrest during pregnancy, including 12 women who underwent perimortem cesarean delivery. In total, only 15 percent (8 of 55) of the women survived. Perimortem cesarean delivery was not associated with a higher survival rate (17 versus 14 percent). However, none of the perimortem cesarean deliveries were performed within the recommended five minutes. Cardiac output was regained in 67 percent (8 of 12) of women after perimortem cesarean delivery; two women (17 percent) and five infants (42 percent) survived.
SUMMARY
The most common causes of cardiopulmonary arrest in pregnant women are pulmonary embolism, amniotic fluid embolism, hemorrhage, sepsis, cardiomyopathy, stroke, preeclampsia-eclampsia, and complications related to anesthesia (eg, difficult or failed intubation, local anesthetic toxicity, aspiration).
Resuscitation of the pregnant women
Cardiac arrest call, which, ideally, activates a multi-disciplinary team
Place firm support under the patient
Modify the ABCs for pregnancy:
Remove fetal and uterine monitoring devices, if present
Displace the uterus laterally and to the left using a wedge or rolled towels/blankets while leaving the upper body supine rather than tilting the entire patient.
Secure the airway using 100 percent oxygen, cricoid pressure, and a slightly smaller endotracheal tube (0.5 mm to 1.0 mm less in internal diameter compared to that used for nonpregnant women).
For chest compressions, hand placement is more cephalad than that used for nonpregnant women. Perform chest compressions slightly above the center of the sternum.
Estimate the gestational age of the fetus (using prenatal record, physical examination, or ultrasound), as it is a factor in the decision making process.
Study suggests perimortem cesarean delivery with delivery of the infant within five minutes of maternal cardiac arrest. Maternal and neonatal outcomes are best when delivery occurs within five minutes of maternal cardiac arrest: normal neurological outcome is possible for both mother and child.
The youtube video below summarises the above topic.
Hypothermic Cardiac Arrest: “no one is dead until warm and dead”
Death from exposure and accidental hypothermia occurs throughout the world and can present significant management problems. Even with modern supportive care, the in-hospital mortality of patients with moderate or severe accidental hypothermia approaches 40 percent.
DEFINITIONS — Hypothermia is defined as a core temperature below 35ºC (95ºF). The stage of hypothermia, defined by core temperature, has a large impact on both recognition and treatment. The most commonly used definitions found in the literature are as follows:
Mild hypothermia – Core temperature 32 to 35ºC (90 to 95ºF)
Moderate hypothermia – Core temperature 28 to 32ºC (82 to 90ºF)
Severe hypothermia – Core temperature below 28ºC (82ºF)
The Swiss staging system is based on clinical signs can be used by rescuers at the scene to describe victims:
Stage I – clearly conscious and shivering;
Stage II – impaired consciousness without shivering;
Stage III – unconscious;
Stage IV – no breathing; and
Stage V – death due to irreversible hypothermia.
MANAGEMENT
For detail management of hypothermic cardiac arrest from European Resus Council, click here
Summary from that guidance:
The risk of hypothermia is increased by drug or alcohol ingestion, exhaustion, illness, injury or neglect especially when there is a decrease in the level of consciousness.
Beware of diagnosing death in a hypothermic patient because cold alone may produce a very slow, small-volume, irregular pulse and unrecordable blood pressure. Dilated pupils can be caused by a variety of insults and must not be regarded as a sign of death.
In the pre-hospital setting, resuscitation should be withheld only if the cause of a cardiac arrest is clearly attributable to a lethal injury, fatal illness, prolonged asphyxia, or if the chest is incompressible.
ABC as usual. Palpate a central artery, look at the ECG (if available), and look for signs of life for up to 1 min before concluding that there is no cardiac output.
Drug metabolism is slowed, leading to potentially toxic plasma concentrations of any drugs given repeatedly. For these reasons, withhold adrenaline and other CPR drugs until the patient has been warmed to a temperature higher than approximately 30 °C. Once 30 °C has been reached, the intervals between drug doses should be doubled when compared with normothermia intervals. As normothermia is approached (over 35 °C), standard drug protocols should be used.
As the body core temperature decreases, sinus bradycardia tends to give way to atrial fibrillation followed by VF and finally asystole.
Arrhythmias other than VF tend to revert spontaneously as the core temperature increases, and usually do not require immediate treatment.
If VF is detected, give a shock at the maximum energy setting; if VF/VT persists after three shocks, delay further defibrillation attempts until the core temperature is above 30 °C.
Rewarming may be passive, active external, or active internal.
In a hypothermic patient with apnoea and cardiac arrest, extracorporeal (ECMO) rewarming is the preferred method of active internal rewarming because it provides sufficient circulation and oxygenation while the core body temperature is increased by 8–12 °C h−1
