Good prognostic factors in schizophrenia include an acute onset, which means that the symptoms appear suddenly and intensely. Additionally, the presence of a precipitating stressful event can also indicate a better prognosis. It is also beneficial if there is no family history of schizophrenia, but a family history of depression can be considered a positive factor. An older age of onset is another good prognostic factor, as it suggests a potentially milder course of the illness. Furthermore, if there is no history of previous episodes and the individual has normal intelligence, it can contribute to a better prognosis. A preponderance of affective symptoms, such as mood-related symptoms, is also considered favorable. It is important to note that the absence of loss of emotion and receiving prompt treatment are additional factors that can improve the prognosis.

In some cases, the signs of skin or mucosal involvement may be difficult to detect or may not be present at all. The Royal College of Emergency Medicine (RCEM) states that anaphylaxis is likely when three specific criteria are met: the illness has a sudden and rapid onset, there are noticeable changes in the skin or mucosal areas such as flushing, hives, or swelling, and there are severe problems with the airway, breathing, or circulation that pose a life-threatening risk.

Further Reading:

Anaphylaxis is a severe and life-threatening hypersensitivity reaction that can have sudden onset and progression. It is characterized by skin or mucosal changes and can lead to life-threatening airway, breathing, or circulatory problems. Anaphylaxis can be allergic or non-allergic in nature.

In allergic anaphylaxis, there is an immediate hypersensitivity reaction where an antigen stimulates the production of IgE antibodies. These antibodies bind to mast cells and basophils. Upon re-exposure to the antigen, the IgE-covered cells release histamine and other inflammatory mediators, causing smooth muscle contraction and vasodilation.

Non-allergic anaphylaxis occurs when mast cells degrade due to a non-immune mediator. The clinical outcome is the same as in allergic anaphylaxis.

The management of anaphylaxis is the same regardless of the cause. Adrenaline is the most important drug and should be administered as soon as possible. The recommended doses for adrenaline vary based on age. Other treatments include high flow oxygen and an IV fluid challenge. Corticosteroids and chlorpheniramine are no longer recommended, while non-sedating antihistamines may be considered as third-line treatment after initial stabilization of airway, breathing, and circulation.

Common causes of anaphylaxis include food (such as nuts, which is the most common cause in children), drugs, and venom (such as wasp stings). Sometimes it can be challenging to determine if a patient had a true episode of anaphylaxis. In such cases, serum tryptase levels may be measured, as they remain elevated for up to 12 hours following an acute episode of anaphylaxis.

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.
https://www.resus.org.uk/sites/default/files/2021-05/Emergency%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf

Haemolytic disease of the newborn is a condition that occurs in the fetus when IgG antibodies from the mother pass through the placenta. This is classified as a type II hypersensitivity reaction, also known as cytotoxic hypersensitivity. In this type of reaction, antibodies produced by the immune response attach to antigens on the patient’s own cell surfaces.

The rhesus gene is composed of three parts, which can be C or c, D or d, and E or e. Approximately 15% of the population consists of rhesus negative women who are homozygous for d. When rhesus-positive fetal cells enter the bloodstream of a rhesus-negative mother, maternal anti-D IgG antibodies may be produced. This commonly occurs during delivery, but can also happen after fetal-maternal hemorrhage and certain medical procedures.

Some other examples of type II hypersensitivity reactions include autoimmune hemolytic anemia, ANCA-associated vasculitides, Goodpasture’s syndrome, myasthenia gravis, and rhesus incompatibility.

If you have missed one pill, which means it has been 48-72 hours since you took the last pill in your current packet or you started the first pill in a new packet 24-48 hours late, you need to take the missed pill as soon as you remember. Make sure to continue taking the remaining pills at your usual time. Emergency contraception is generally not necessary in this situation, but it may be worth considering if you have missed pills earlier in the packet or during the last week of the previous packet.

Ulcerative colitis is a condition that is less common among smokers, as around 70-80% of individuals affected by this disease are non-smokers. There are several recognized associations of ulcerative colitis, including aphthous ulcers, uveitis and episcleritis, seronegative spondyloarthropathies, sacroiliitis, erythema nodosum, pyoderma gangrenosum, finger clubbing, autoimmune hemolytic anemia, primary biliary cirrhosis, primary sclerosing cholangitis, and chronic active hepatitis. These conditions often coexist with ulcerative colitis and can provide additional insight into the disease.

Metastatic spinal cord compression (MSCC) occurs when a tumor mass compresses the thecal sac and its components, leading to a spinal emergency. If the pressure on the spinal cord is not relieved promptly, it can result in irreversible loss of neurological function. The most crucial factor for predicting functional outcome is the patient’s neurological function before treatment. Therefore, delayed treatment can lead to permanent disability and a decrease in quality of life.

The most common cancers that cause MSCC are prostate, lung, breast, and myeloma. In approximately 10 to 20% of cancer patients, MSCC is the first noticeable symptom. It is important to consider MSCC in any patient with a history of cancer if they experience any of the following symptoms: severe or progressive lumbar back pain, nocturnal pain that disrupts sleep, localized spinal tenderness, radicular pain, or neurological symptoms.

Thoracic pain can also be an indicator of MSCC, but it can also be caused by an aortic aneurysm. In patients aged 60 or older with persistent back pain, myeloma should be considered. Similarly, in patients aged 60 or older with accompanying weight loss, pancreatic cancer should be considered.

Functional murmurs, also referred to as physiological or flow murmurs, are frequently observed during pregnancy and other conditions associated with increased blood flow. These murmurs arise as a result of the heightened resting cardiac output and do not necessitate any additional examination.

ST elevation and ventricular ectopics indicate that the needle has made contact with the ventricle. In such cases, it is recommended to retract the needle until the ECG pattern returns to its normal baseline.

Further Reading:

Cardiac tamponade, also known as pericardial tamponade, occurs when fluid accumulates in the pericardial sac and compresses the heart, leading to compromised blood flow. Classic clinical signs of cardiac tamponade include distended neck veins, hypotension, muffled heart sounds, and pulseless electrical activity (PEA). Diagnosis is typically done through a FAST scan or an echocardiogram.

Management of cardiac tamponade involves assessing for other injuries, administering IV fluids to reduce preload, performing pericardiocentesis (inserting a needle into the pericardial cavity to drain fluid), and potentially performing a thoracotomy. It is important to note that untreated expanding cardiac tamponade can progress to PEA cardiac arrest.

Pericardiocentesis can be done using the subxiphoid approach or by inserting a needle between the 5th and 6th intercostal spaces at the left sternal border. Echo guidance is the gold standard for pericardiocentesis, but it may not be available in a resuscitation situation. Complications of pericardiocentesis include ST elevation or ventricular ectopics, myocardial perforation, bleeding, pneumothorax, arrhythmia, acute pulmonary edema, and acute ventricular dilatation.

It is important to note that pericardiocentesis is typically used as a temporary measure until a thoracotomy can be performed. Recent articles published on the RCEM learning platform suggest that pericardiocentesis has a low success rate and may delay thoracotomy, so it is advised against unless there are no other options available.

Whooping cough, also known as pertussis, is a respiratory infection caused by the bacteria Bordetella pertussis. It is transmitted through respiratory droplets and has an incubation period of about 7-21 days. This highly contagious disease can be passed on to around 90% of close household contacts.

To prevent the spread of whooping cough, Public Health England advises that children with the illness should stay away from school, nursery, or childminders for 48 hours after starting antibiotic treatment. If no antibiotic treatment is given, they should be kept away for 21 days from the onset of the illness. It’s important to note that even after treatment, non-infectious coughing may persist for several weeks.

For more information on how to control infections in schools and other childcare settings, you can refer to the guidance provided by Public Health England.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting around 5% of patients over the age of 70-75 years and 10% of patients aged 80-85 years. While AF can cause palpitations and inefficient cardiac function, the most important aspect of managing patients with AF is reducing the increased risk of stroke.

AF can be classified as first detected episode, paroxysmal, persistent, or permanent. First detected episode refers to the initial occurrence of AF, regardless of symptoms or duration. Paroxysmal AF occurs when a patient has 2 or more self-terminating episodes lasting less than 7 days. Persistent AF refers to episodes lasting more than 7 days that do not self-terminate. Permanent AF is continuous atrial fibrillation that cannot be cardioverted or if attempts to do so are deemed inappropriate. The treatment goals for permanent AF are rate control and anticoagulation if appropriate.

Symptoms of AF include palpitations, dyspnea, and chest pain. The most common sign is an irregularly irregular pulse. An electrocardiogram (ECG) is essential for diagnosing AF, as other conditions can also cause an irregular pulse.

Managing patients with AF involves two key parts: rate/rhythm control and reducing stroke risk. Rate control involves slowing down the irregular pulse to avoid negative effects on cardiac function. This is typically achieved using beta-blockers or rate-limiting calcium channel blockers. If one drug is not effective, combination therapy may be used. Rhythm control aims to restore and maintain normal sinus rhythm through pharmacological or electrical cardioversion. However, the majority of patients are managed with a rate control strategy.

Reducing stroke risk in patients with AF is crucial. Risk stratifying tools, such as the CHA2DS2-VASc score, are used to determine the most appropriate anticoagulation strategy. Anticoagulation is recommended for patients with a score of 2 or more. Clinicians can choose between warfarin and novel oral anticoagulants (NOACs) for anticoagulation.

Before starting anticoagulation, the patient’s bleeding risk should be assessed using tools like the HAS-BLED score or the ORBIT tool. These tools evaluate factors such as hypertension, abnormal renal or liver function, history of bleeding, age, and use of drugs that predispose to bleeding.

The recommended diagnostic tests for Cushing’s syndrome include the 24-hour urinary free cortisol test, the 1 mg overnight dexamethasone suppression test, and the late-night salivary cortisol test. In this case, the patient exhibits symptoms of Cushing syndrome such as a moon face, abdominal striae, and hirsutism. These symptoms may be caused by Cushing’s disease, which is Cushing syndrome due to a pituitary adenoma. The patient also experiences headaches and visual disturbances, which could potentially be caused by high blood sugar levels. It is important to note that Cushing syndrome caused by an adrenal or pituitary tumor is more common in females, with a ratio of 5:1. The peak incidence of Cushing syndrome caused by an adrenal or pituitary adenoma occurs between the ages of 25 and 40 years.

Further Reading:

Cushing’s syndrome is a clinical syndrome caused by prolonged exposure to high levels of glucocorticoids. The severity of symptoms can vary depending on the level of steroid exposure. There are two main classifications of Cushing’s syndrome: ACTH-dependent disease and non-ACTH-dependent disease. ACTH-dependent disease is caused by excessive ACTH production from the pituitary gland or ACTH-secreting tumors, which stimulate excessive cortisol production. Non-ACTH-dependent disease is characterized by excess glucocorticoid production independent of ACTH stimulation.

The most common cause of Cushing’s syndrome is exogenous steroid use. Pituitary adenoma is the second most common cause and the most common endogenous cause. Cushing’s disease refers specifically to Cushing’s syndrome caused by an ACTH-producing pituitary tumor.

Clinical features of Cushing’s syndrome include truncal obesity, supraclavicular fat pads, buffalo hump, weight gain, moon facies, muscle wasting and weakness, diabetes or impaired glucose tolerance, gonadal dysfunction, hypertension, nephrolithiasis, skin changes (such as skin atrophy, striae, easy bruising, hirsutism, acne, and hyperpigmentation in ACTH-dependent causes), depression and emotional lability, osteopenia or osteoporosis, edema, irregular menstrual cycles or amenorrhea, polydipsia and polyuria, poor wound healing, and signs related to the underlying cause, such as headaches and visual problems.

Diagnostic tests for Cushing’s syndrome include 24-hour urinary free cortisol, 1 mg overnight dexamethasone suppression test, and late-night salivary cortisol. Other investigations aim to assess metabolic disturbances and identify the underlying cause, such as plasma ACTH, full blood count (raised white cell count), electrolytes, and arterial blood gas analysis. Imaging, such as CT or MRI of the abdomen, chest, and/or pituitary, may be required to assess suspected adrenal tumors, ectopic ACTH-secreting tumors, and pituitary tumors. The choice of imaging is guided by the ACTH result, with undetectable ACTH and elevated serum cortisol levels indicating ACTH-independent Cushing’s syndrome and raised ACTH suggesting an ACTH-secreting tumor.

Ketamine primarily works by blocking NMDA receptors, although its complete mechanism of action is not yet fully comprehended. Ongoing research is exploring its impact on various other receptors.

Further Reading:

Procedural sedation is commonly used by emergency department (ED) doctors to minimize pain and discomfort during procedures that may be painful or distressing for patients. Effective procedural sedation requires the administration of analgesia, anxiolysis, sedation, and amnesia. This is typically achieved through the use of a combination of short-acting analgesics and sedatives.

There are different levels of sedation, ranging from minimal sedation (anxiolysis) to general anesthesia. It is important for clinicians to understand the level of sedation being used and to be able to manage any unintended deeper levels of sedation that may occur. Deeper levels of sedation are similar to general anesthesia and require the same level of care and monitoring.

Various drugs can be used for procedural sedation, including propofol, midazolam, ketamine, and fentanyl. Each of these drugs has its own mechanism of action and side effects. Propofol is commonly used for sedation, amnesia, and induction and maintenance of general anesthesia. Midazolam is a benzodiazepine that enhances the effect of GABA on the GABA A receptors. Ketamine is an NMDA receptor antagonist and is used for dissociative sedation. Fentanyl is a highly potent opioid used for analgesia and sedation.

The doses of these drugs for procedural sedation in the ED vary depending on the drug and the route of administration. It is important for clinicians to be familiar with the appropriate doses and onset and peak effect times for each drug.

Safe sedation requires certain requirements, including appropriate staffing levels, competencies of the sedating practitioner, location and facilities, and monitoring. The level of sedation being used determines the specific requirements for safe sedation.

After the procedure, patients should be monitored until they meet the criteria for safe discharge. This includes returning to their baseline level of consciousness, having vital signs within normal limits, and not experiencing compromised respiratory status. Pain and discomfort should also be addressed before discharge.

According to NICE, the presence of certain clinical features in a child between three months and five years old may indicate a urinary tract infection (UTI). These features include vomiting, poor feeding, lethargy, irritability, abdominal pain or tenderness, and urinary frequency or dysuria. For more information on this topic, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

The superior orbital fissure is a gap in the back wall of the orbit, created by the space between the greater and lesser wings of the sphenoid bone. Several structures pass through it to enter the orbit, starting from the top and going downwards. These include the lacrimal nerve (a branch of CN V1), the frontal nerve (another branch of CN V1), the superior ophthalmic vein, the trochlear nerve (CN IV), the superior division of the oculomotor nerve (CN III), the nasociliary nerve (a branch of CN V1), the inferior division of the oculomotor nerve (CN III), the abducens nerve (CN VI), and the inferior ophthalmic vein.

Adjacent to the superior orbital fissure, on the back wall of the orbit and towards the middle, is the optic canal. The optic nerve (CN II) exits the orbit through this canal, along with the ophthalmic artery.

Superior orbital fissure syndrome (SOFS) is a condition characterized by a combination of symptoms and signs that occur when cranial nerves III, IV, V1, and VI are compressed or injured as they pass through the superior orbital fissure. This condition also leads to swelling and protrusion of the eye due to impaired drainage and congestion. The main causes of SOFS are trauma, tumors, and inflammation. It is important to note that CN II is not affected by this syndrome, as it follows a separate path through the optic canal.

Anaphylaxis, also known as anaphylactic shock, is characterized by certain symptoms similar to other types of shock. These symptoms include low blood pressure (hypotension), rapid heart rate (tachycardia), irregular heart rhythm (arrhythmia), changes in the electrocardiogram (ECG) indicating reduced blood flow to the heart (myocardial ischemia), such as ST elevation, and in severe cases, cardiac arrest.

Further Reading:

Anaphylaxis is a severe and life-threatening hypersensitivity reaction that can have sudden onset and progression. It is characterized by skin or mucosal changes and can lead to life-threatening airway, breathing, or circulatory problems. Anaphylaxis can be allergic or non-allergic in nature.

In allergic anaphylaxis, there is an immediate hypersensitivity reaction where an antigen stimulates the production of IgE antibodies. These antibodies bind to mast cells and basophils. Upon re-exposure to the antigen, the IgE-covered cells release histamine and other inflammatory mediators, causing smooth muscle contraction and vasodilation.

Non-allergic anaphylaxis occurs when mast cells degrade due to a non-immune mediator. The clinical outcome is the same as in allergic anaphylaxis.

The management of anaphylaxis is the same regardless of the cause. Adrenaline is the most important drug and should be administered as soon as possible. The recommended doses for adrenaline vary based on age. Other treatments include high flow oxygen and an IV fluid challenge. Corticosteroids and chlorpheniramine are no longer recommended, while non-sedating antihistamines may be considered as third-line treatment after initial stabilization of airway, breathing, and circulation.

Common causes of anaphylaxis include food (such as nuts, which is the most common cause in children), drugs, and venom (such as wasp stings). Sometimes it can be challenging to determine if a patient had a true episode of anaphylaxis. In such cases, serum tryptase levels may be measured, as they remain elevated for up to 12 hours following an acute episode of anaphylaxis.

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.
https://www.resus.org.uk/sites/default/files/2021-05/Emergency%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf

Zygomaticomaxillary complex fractures, also known as quadramalar or tripod fractures, make up around 40% of all midface fractures and are the second most common facial bone fractures after nasal bone fractures.

These injuries typically occur when a direct blow is delivered to the malar eminence of the cheek. They consist of four components:

1. Widening of the zygomaticofrontal suture
2. Fracture of the zygomatic arch
3. Fracture of the inferior orbital rim and the walls of the anterior and posterior maxillary sinuses
4. Fracture of the lateral orbital rim.

The symptoms observed in the casualties of this CBRN event strongly indicate exposure to a nerve agent. Among the options provided, VX gas is the only nerve agent listed, making it the most likely culprit.

Nerve agents, also known as nerve gases, are a highly toxic group of chemical warfare agents that were developed just before and during World War II. The initial compounds in this category, known as the G agents, were discovered and synthesized by German scientists. They include Tabun (GA), Sarin (GB), and Soman (GD). In the 1950s, the V agents, which are approximately 10 times more poisonous than Sarin, were synthesized. These include Venomous agent X (VX), Venomous agent E (VE), Venomous agent G (VG), and Venomous agent M (VM).

One of the most well-known incidents involving a nerve agent was the Tokyo subway sarin attack in March 1995. During this attack, Sarin was released into the Tokyo subway system during rush hour, resulting in over 5,000 people seeking medical attention. Among them, 984 were moderately poisoned, 54 were severely poisoned, and 12 lost their lives.

Nerve agents are organophosphorus esters that are chemically related to organophosphorus insecticides. They work by inhibiting acetylcholinesterase (AChE), an enzyme responsible for breaking down the neurotransmitter acetylcholine (ACh). This inhibition leads to an accumulation of ACh at both muscarinic and nicotinic cholinergic receptors.

Nerve agents can be absorbed through any body surface. When dispersed as a spray or aerosol, they can enter the body through the skin, eyes, and respiratory tract. In vapor form, they are primarily absorbed through the respiratory tract and eyes. If a sufficient amount of the agent is absorbed, it can cause local effects followed by systemic effects throughout the body.

The clinical symptoms observed after exposure to nerve agents are a result of the combined effects on the muscarinic, nicotinic, and central nervous systems. Muscarinic effects, often remembered using the acronym DUMBBELS, include diarrhea, urination, miosis (constriction of the pupils), bronchorrhea (excessive mucus production in the airways), bronchospasm (narrowing of the airways), emesis (vomiting), lacrimation (excessive tearing), and salivation.

One of the signs of digoxin toxicity is yellow-green vision. Other clinical features include feeling generally unwell, lethargy, nausea and vomiting, loss of appetite, confusion, and the development of arrhythmias such as AV block and bradycardia.

Further Reading:

Digoxin is a medication used for rate control in atrial fibrillation and for improving symptoms in heart failure. It works by decreasing conduction through the atrioventricular node and increasing the force of cardiac muscle contraction. However, digoxin toxicity can occur, and plasma concentration alone does not determine if a patient has developed toxicity. Symptoms of digoxin toxicity include feeling generally unwell, lethargy, nausea and vomiting, anorexia, confusion, yellow-green vision, arrhythmias, and gynaecomastia.

ECG changes seen in digoxin toxicity include downsloping ST depression with a characteristic Salvador Dali sagging appearance, flattened, inverted, or biphasic T waves, shortened QT interval, mild PR interval prolongation, and prominent U waves. There are several precipitating factors for digoxin toxicity, including hypokalaemia, increasing age, renal failure, myocardial ischaemia, electrolyte imbalances, hypoalbuminaemia, hypothermia, hypothyroidism, and certain medications such as amiodarone, quinidine, verapamil, and diltiazem.

Management of digoxin toxicity involves the use of digoxin specific antibody fragments, also known as Digibind or digifab. Arrhythmias should be treated, and electrolyte disturbances should be corrected with close monitoring of potassium levels. It is important to note that digoxin toxicity can be precipitated by hypokalaemia, and toxicity can then lead to hyperkalaemia.

Angiotensin-converting enzyme (ACE) inhibitors are the primary cause of drug-induced angioedema in the UK and USA, mainly due to their widespread use. The incidence of angioedema caused by ACE inhibitors ranges from 0.1 to 0.7% among recipients, with evidence suggesting a consistent and persistent risk each year. Interestingly, individuals of African descent are approximately five times more likely to experience this adverse reaction.

The most common symptoms observed in patients with ACE inhibitor-induced angioedema include swelling of the lips, tongue, or face. However, another manifestation of this condition is episodic abdominal pain caused by intestinal angioedema. Notably, urticaria (hives) and itching are absent in these cases.

The underlying mechanism of ACE inhibitor-induced angioedema appears to involve the activation of the complement system or other pro-inflammatory cytokines, such as prostaglandins and histamine. These substances trigger rapid dilation of blood vessels and the accumulation of fluid, leading to edema.

Although less frequently associated with angioedema, other medications that may cause this condition include angiotensin-receptor blockers (ARBs), nonsteroidal anti-inflammatory drugs (NSAIDs), bupropion (e.g., Zyban and Wellbutrin), beta-lactam antibiotics, statins, and proton pump inhibitors.

Fortunately, most cases of drug-induced angioedema are mild and can be effectively managed by discontinuing the medication and prescribing oral antihistamines.

The diagnosis in this case is clearly gout. According to the European League Against Rheumatism (EULAR) guidelines, the development of sudden joint pain accompanied by swelling, tenderness, and redness, which worsens over a period of 6-12 hours, strongly suggests crystal arthropathy.

Checking serum urate levels to confirm high levels of uric acid before starting treatment for acute gout attacks is not very beneficial and should not delay treatment. While these levels can be useful for monitoring treatment response, they often decrease during an acute attack and can even be normal. If levels are checked and found to be normal during an attack, they should be rechecked once the attack has resolved.

The first-line treatment for acute gout attacks is non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen. However, caution should be exercised when using NSAIDs in patients with a history of hypertension. Since this patient has had difficulty controlling their blood pressure and remains hypertensive, it would be wise to avoid NSAIDs in this case.

Colchicine is an effective alternative for treating gout, although it may take longer to take effect. It is often used in patients who cannot take NSAIDs due to contraindications, such as hypertension or a history of peptic ulcer disease. It’s important to note that colchicine can also affect the bone marrow, leading to an increase in white blood cells and a decrease in platelets. Therefore, it should not be used in patients with blood disorders, as in this case.

During an acute gout attack, allopurinol should not be used as it can prolong the attack and even trigger another acute attack. If a patient is already taking allopurinol, it should be continued, and the acute attack should be treated with NSAIDs, colchicine, or corticosteroids as appropriate.

Corticosteroids are an effective alternative for managing acute gout in patients who cannot take NSAIDs or colchicine. They can be administered orally, intramuscularly, intravenously, or directly into the affected joint. In this patient’s case, using corticosteroids would be the safest and most reasonable treatment option.