The intravascular volume of an infant is approximately 80 ml/kg, while in older children it is around 70 ml/kg. Dehydration itself does not lead to death, but shock can. Shock can occur when there is a loss of 20 ml/kg from the intravascular space, whereas clinical dehydration is only noticeable after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children based on their body weight:

Bodyweight: First 10 kg
Daily fluid requirement: 100 ml/kg
Hourly fluid requirement: 4 ml/kg

Bodyweight: Second 10 kg
Daily fluid requirement: 50 ml/kg
Hourly fluid requirement: 2 ml/kg

Bodyweight: Subsequent kg
Daily fluid requirement: 20 ml/kg
Hourly fluid requirement: 1 ml/kg

In general, if a child shows clinical signs of dehydration without shock, they can be assumed to be 5% dehydrated. If shock is also present, it can be assumed that they are 10% dehydrated or more. 5% dehydration means that the body has lost 5 g per 100 g body weight, which is equivalent to 50 ml/kg of fluid. Therefore, 10% dehydration implies a loss of 100 ml/kg of fluid.

In the case of this child, they are in shock and should receive a 20 ml/kg fluid bolus. Therefore, the initial volume of fluid to administer should be 20 x 8 ml = 160 ml.

The clinical features of dehydration and shock are summarized in the table below:

Dehydration (5%):
– Appears ‘unwell’
– Normal heart rate or tachycardia
– Normal respiratory rate or tachypnea
– Normal peripheral pulses
– Normal or mildly prolonged capillary refill time (CRT)
– Normal blood pressure
– Warm extremities
– Decreased urine output
– Reduced skin turgor
– Sunken eyes
– Depressed fontanelle
– Dry mucous membranes

Clinical shock (10%):
– Pale, lethargic, mottled appearance
– Tachycardia
– Tachypnea
– Weak peripheral pulses
– Prolonged capillary refill time (CRT)
– Hypotension
– Cold extremities
– Decreased urine output
– Decreased level of consciousness

Sodium bicarbonate is used to treat severe TCA toxicity by reducing the risk of seizures and arrhythmia. The goal is to increase the serum pH to a range of 7.45 to 7.55 through alkalinisation.

Further Reading:

Tricyclic antidepressant (TCA) overdose is a common occurrence in emergency departments, with drugs like amitriptyline and dosulepin being particularly dangerous. TCAs work by inhibiting the reuptake of norepinephrine and serotonin in the central nervous system. In cases of toxicity, TCAs block various receptors, including alpha-adrenergic, histaminic, muscarinic, and serotonin receptors. This can lead to symptoms such as hypotension, altered mental state, signs of anticholinergic toxicity, and serotonin receptor effects.

TCAs primarily cause cardiac toxicity by blocking sodium and potassium channels. This can result in a slowing of the action potential, prolongation of the QRS complex, and bradycardia. However, the blockade of muscarinic receptors also leads to tachycardia in TCA overdose. QT prolongation and Torsades de Pointes can occur due to potassium channel blockade. TCAs can also have a toxic effect on the myocardium, causing decreased cardiac contractility and hypotension.

Early symptoms of TCA overdose are related to their anticholinergic properties and may include dry mouth, pyrexia, dilated pupils, agitation, sinus tachycardia, blurred vision, flushed skin, tremor, and confusion. Severe poisoning can lead to arrhythmias, seizures, metabolic acidosis, and coma. ECG changes commonly seen in TCA overdose include sinus tachycardia, widening of the QRS complex, prolongation of the QT interval, and an R/S ratio >0.7 in lead aVR.

Management of TCA overdose involves ensuring a patent airway, administering activated charcoal if ingestion occurred within 1 hour and the airway is intact, and considering gastric lavage for life-threatening cases within 1 hour of ingestion. Serial ECGs and blood gas analysis are important for monitoring. Intravenous fluids and correction of hypoxia are the first-line therapies. IV sodium bicarbonate is used to treat haemodynamic instability caused by TCA overdose, and benzodiazepines are the treatment of choice for seizure control. Other treatments that may be considered include glucagon, magnesium sulfate, and intravenous lipid emulsion.

There are certain things to avoid in TCA overdose, such as anti-arrhythmics like quinidine and flecainide, as they can prolonged depolarization.

Isoniazid has the potential to induce acute hepatitis, but it is not considered a known cause of cholestatic jaundice. On the other hand, there are several drugs that have been identified as culprits for cholestatic jaundice. These include nitrofurantoin, erythromycin, cephalosporins, verapamil, NSAIDs, ACE inhibitors, tricyclic antidepressants, phenytoin, azathioprine, carbamazepine, oral contraceptive pills, diazepam, ketoconazole, and tamoxifen. It is important to be aware of these medications and their potential side effects in order to ensure patient safety.

Bell’s palsy is a condition characterized by a facial paralysis that affects the lower motor neurons. It can be distinguished from an upper motor neuron lesion by the individual’s inability to raise their eyebrow and the involvement of the upper facial muscles.

One notable feature of Bell’s palsy is the occurrence of Bell’s phenomenon, which refers to the upward and outward rolling of the eye on the affected side when attempting to close the eye and bare the teeth.

Approximately 80% of sudden onset lower motor neuron facial palsies are attributed to Bell’s palsy. It is believed that this condition is caused by swelling of the facial nerve within the petrous temporal bone, which is thought to be a result of a latent herpesvirus, specifically HSV-1 and HZV.

Treatment for Bell’s palsy often involves the use of steroids and acyclovir. These medications can help alleviate symptoms and promote recovery.

Vestibular neuronitis is characterized by the sudden and prolonged onset of rotational vertigo. This vertigo can occur spontaneously, upon waking up, or gradually worsen throughout the day. It is particularly aggravated by changes in head position, although it remains constant even when the head is still. Unlike other conditions, vestibular neuronitis does not cause hearing loss, tinnitus, or focal neurological deficits. On the other hand, in BPPV, episodes of vertigo are usually brief, lasting less than 20 seconds, and only occur when there is a change in head position.

Further Reading:

Vestibular neuritis, also known as vestibular neuronitis, is a condition characterized by sudden and prolonged vertigo of peripheral origin. It is believed to be caused by inflammation of the vestibular nerve, often following a viral infection. It is important to note that vestibular neuritis and labyrinthitis are not the same condition, as labyrinthitis involves inflammation of the labyrinth. Vestibular neuritis typically affects individuals between the ages of 30 and 60, with a 1:1 ratio of males to females. The annual incidence is approximately 3.5 per 100,000 people, making it one of the most commonly diagnosed causes of vertigo.

Clinical features of vestibular neuritis include nystagmus, which is a rapid, involuntary eye movement, typically in a horizontal or horizontal-torsional direction away from the affected ear. The head impulse test may also be positive. Other symptoms include spontaneous onset of rotational vertigo, which is worsened by changes in head position, as well as nausea, vomiting, and unsteadiness. These severe symptoms usually last for 2-3 days, followed by a gradual recovery over a few weeks. It is important to note that hearing is not affected in vestibular neuritis, and symptoms such as tinnitus and focal neurological deficits are not present.

Differential diagnosis for vestibular neuritis includes benign paroxysmal positional vertigo (BPPV), labyrinthitis, Meniere’s disease, migraine, stroke, and cerebellar lesions. Management of vestibular neuritis involves drug treatment for nausea and vomiting associated with vertigo, typically through short courses of medication such as prochlorperazine or cyclizine. If symptoms are severe and fluids cannot be tolerated, admission and administration of IV fluids may be necessary. General advice should also be given, including avoiding driving while symptomatic, considering the suitability to work based on occupation and duties, and the increased risk of falls. Follow-up is required, and referral is necessary if there are atypical symptoms, symptoms do not improve after a week of treatment, or symptoms persist for more than 6 weeks.

The prognosis for vestibular neuritis is generally good, with the majority of individuals fully recovering within 6 weeks. Recurrence is thought to occur in 2-11% of cases, and approximately 10% of individuals may develop BPPV following an episode of vestibular neuritis. A very rare complication of vestibular neuritis is ph

Thiazide diuretics, like bendroflumethiazide and hydrochlorothiazide, have the potential to raise levels of uric acid in the blood, which can worsen gout symptoms in individuals who are susceptible to the condition.

Other medications, such as diuretics, beta-blockers, ACE inhibitors, and non-losartan ARBs, are also linked to an increased risk of gout.

On the other hand, calcium-channel blockers like amlodipine and verapamil, as well as losartan, have been found to lower uric acid levels and are associated with a reduced risk of gout.

Dexamethasone is the preferred medication for treating Acute Mountain Sickness (AMS) and High Altitude Cerebral Edema (HACE). In cases of mild AMS, simply halting the ascent and giving the body time to acclimatize may be sufficient. However, if mild AMS persists or worsens, or if the patient experiences moderate to severe AMS, descending to a lower altitude is the most effective treatment, preferably with the addition of supplemental oxygen. Dexamethasone is the recommended medication for managing both AMS and HACE.

Further Reading:

High Altitude Illnesses

Altitude & Hypoxia:
– As altitude increases, atmospheric pressure decreases and inspired oxygen pressure falls.
– Hypoxia occurs at altitude due to decreased inspired oxygen.
– At 5500m, inspired oxygen is approximately half that at sea level, and at 8900m, it is less than a third.

Acute Mountain Sickness (AMS):
– AMS is a clinical syndrome caused by hypoxia at altitude.
– Symptoms include headache, anorexia, sleep disturbance, nausea, dizziness, fatigue, malaise, and shortness of breath.
– Symptoms usually occur after 6-12 hours above 2500m.
– Risk factors for AMS include previous AMS, fast ascent, sleeping at altitude, and age <50 years old.
– The Lake Louise AMS score is used to assess the severity of AMS.
– Treatment involves stopping ascent, maintaining hydration, and using medication for symptom relief.
– Medications for moderate to severe symptoms include dexamethasone and acetazolamide.
– Gradual ascent, hydration, and avoiding alcohol can help prevent AMS.

High Altitude Pulmonary Edema (HAPE):
– HAPE is a progression of AMS but can occur without AMS symptoms.
– It is the leading cause of death related to altitude illness.
– Risk factors for HAPE include rate of ascent, intensity of exercise, absolute altitude, and individual susceptibility.
– Symptoms include dyspnea, cough, chest tightness, poor exercise tolerance, cyanosis, low oxygen saturations, tachycardia, tachypnea, crepitations, and orthopnea.
– Management involves immediate descent, supplemental oxygen, keeping warm, and medication such as nifedipine.

High Altitude Cerebral Edema (HACE):
– HACE is thought to result from vasogenic edema and increased vascular pressure.
– It occurs 2-4 days after ascent and is associated with moderate to severe AMS symptoms.
– Symptoms include headache, hallucinations, disorientation, confusion, ataxia, drowsiness, seizures, and manifestations of raised intracranial pressure.
– Immediate descent is crucial for management, and portable hyperbaric therapy may be used if descent is not possible.
– Medication for treatment includes dexamethasone and supplemental oxygen. Acetazolamide is typically used for prophylaxis.

HIV is currently not considered a notifiable disease. The Health Protection (Notification) Regulations require the reporting of certain diseases, but HIV is not included in this list. The diseases that are currently considered notifiable include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhea, invasive group A streptococcal disease, Legionnaires’ Disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, SARS, scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever. If you want to learn more about notifiable diseases and the organisms that cause them, you can refer to the Notifiable diseases and causative organisms: how to report resource.

This patient has developed Wernicke’s encephalopathy, a condition that is associated with alcohol abuse and other causes of thiamine deficiency. It is important to note that the infusion of glucose-containing intravenous fluids without thiamine in a patient with chronic thiamine deficiency can trigger Wernicke’s encephalopathy. In this particular case, it seems that this is what has occurred.

Wernicke’s encephalopathy is typically characterized by a triad of symptoms, which include acute confusion, ophthalmoplegia, and ataxia. Additionally, other possible features of this condition may include papilloedema, hearing loss, apathy, dysphagia, memory impairment, and hypothermia. It is also common for peripheral neuropathy, primarily affecting the legs, to occur in the majority of cases.

This condition is characterized by the presence of acute capillary haemorrhages, astrocytosis, and neuronal death in the upper brainstem and diencephalon. These abnormalities can be visualized through MRI scanning, although CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will go on to develop a Korsakoff psychosis. This condition is characterized by retrograde amnesia, an inability to form new memories, disordered time perception, and confabulation.

Patients who are suspected to have Wernicke’s encephalopathy should be promptly treated with parenteral thiamine (such as Pabrinex) for a minimum of 5 days. Following the parenteral therapy, oral thiamine should be administered.

This patient has been diagnosed with primary biliary cirrhosis (PBC). PBC is a liver disease caused by an autoimmune response, leading to the progressive destruction of the small bile ducts in the liver. The damage primarily affects the intralobular ducts. As a result, the patient experiences cholestatic jaundice, followed by liver fibrosis and cirrhosis. PBC is more common in females, with 90% of patients being women. It typically occurs between the ages of 30 and 65. Liver function tests show elevated levels of alkaline phosphatase (ALP), often before any symptoms appear. Antimitochondrial antibodies are positive in 95% of cases. Around 50% of patients have smooth muscle antibodies (SMA), and approximately 20% have antinuclear antibodies (ANA). IgM levels are raised in over 80% of cases.

Autoimmune hepatitis is liver inflammation caused by a decrease in regulatory T-cells (Treg cells), leading to the production of autoantibodies against hepatocyte surface antigens. It mainly affects women (70%) between the ages of 15 and 40. The condition causes chronic, progressive hepatitis, which eventually progresses to cirrhosis. Patients typically present with non-specific symptoms of malaise, although in some cases, the disease may be more advanced, resulting in jaundice and severe illness. In later stages, liver function tests show significantly elevated levels of transaminases (ALT and AST), often exceeding ten times the normal range. Alkaline phosphatase (ALP) levels are usually normal or slightly elevated. Antinuclear antibodies (ANA) are positive in approximately 80% of cases, while smooth muscle antibodies (SMA) are positive in around 70% of cases. Antimitochondrial antibodies are typically low or absent.

Primary sclerosing cholangitis (PSC) is a condition that causes progressive inflammation and obstruction of the bile ducts. It is characterized by recurrent episodes of cholangitis and the gradual scarring of the bile ducts. PSC can eventually lead to liver cirrhosis, liver failure, and hepatocellular carcinoma. There is a known association between PSC and ulcerative colitis, with over 80% of PSC patients also having ulcerative colitis.

Hepatic damage caused by hydroxychloroquine is extremely rare.

Pertussis, also known as whooping cough, is a respiratory infection caused by the bacteria Bordetella pertussis. Despite being a bacterial disease, antibiotics do not change the course of the illness once it has taken hold. However, macrolide antibiotics have been proven to shorten the period of contagiousness. Therefore, it is important to administer antibiotics as soon as possible after the onset of symptoms to eliminate the bacteria and reduce further transmission. It is crucial to start antibiotics within three weeks of symptom onset, as they do not affect the progression of the illness or the contagious period.

First-line treatment for pertussis includes macrolide antibiotics. For babies under one month old, clarithromycin is recommended. For children one month and older, as well as non-pregnant adults, azithromycin or clarithromycin are the preferred options. Pregnant women should be treated with erythromycin. In cases where macrolides are not suitable or well-tolerated, co-trimoxazole can be used off-label.

Blood transfusion is a crucial treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion use, errors and adverse reactions still occur.

Delayed haemolytic transfusion reactions (DHTRs) typically occur 4-8 days after a blood transfusion, but can sometimes manifest up to a month later. The symptoms are similar to acute haemolytic transfusion reactions but are usually less severe. Patients may experience fever, inadequate rise in haemoglobin, jaundice, reticulocytosis, positive antibody screen, and positive Direct Antiglobulin Test (Coombs test). DHTRs are more common in patients with sickle cell disease who have received frequent transfusions.

These reactions are caused by the presence of a low titre antibody that is too weak to be detected during cross-match and unable to cause lysis at the time of transfusion. The severity of DHTRs depends on the immunogenicity or dose of the antigen. Blood group antibodies associated with DHTRs include those of the Kidd, Duffy, Kell, and MNS systems. Most DHTRs have a benign course and do not require treatment. However, severe haemolysis with anaemia and renal failure can occur, so monitoring of haemoglobin levels and renal function is necessary. If an antibody is detected, antigen-negative blood can be requested for future transfusions.

Here is a summary of the main transfusion reactions and complications:

1. Febrile transfusion reaction: Presents with a 1-degree rise in temperature from baseline, along with chills and malaise. It is the most common reaction and is usually caused by cytokines from leukocytes in transfused red cell or platelet components. Supportive treatment with paracetamol is helpful.

2. Acute haemolytic reaction: Symptoms include fever, chills, pain at the transfusion site, nausea, vomiting, and dark urine. It is the most serious type of reaction and often occurs due to ABO incompatibility from administration errors. The transfusion should be stopped, and IV fluids should be administered. Diuretics may be required.

3. Delayed haemolytic reaction: This reaction typically occurs 4-8 days after a blood transfusion and presents with fever, anaemia, jaundice and haemoglobuinuria. Direct antiglobulin (Coombs) test positive. Due to low titre antibody too weak to detect in cross-match and unable to cause lysis at time of transfusion. Most delayed haemolytic reactions have a benign course and require no treatment. Monitor anaemia and renal function and treat as required.

The recommended dose of adrenaline is 7 mg per kilogram of body weight, with a maximum limit of 500 mg.

Local anaesthetics, such as lidocaine, bupivacaine, and prilocaine, are commonly used in the emergency department for topical or local infiltration to establish a field block. Lidocaine is often the first choice for field block prior to central line insertion. These anaesthetics work by blocking sodium channels, preventing the propagation of action potentials.

However, local anaesthetics can enter the systemic circulation and cause toxic side effects if administered in high doses. Clinicians must be aware of the signs and symptoms of local anaesthetic systemic toxicity (LAST) and know how to respond. Early signs of LAST include numbness around the mouth or tongue, metallic taste, dizziness, visual and auditory disturbances, disorientation, and drowsiness. If not addressed, LAST can progress to more severe symptoms such as seizures, coma, respiratory depression, and cardiovascular dysfunction.

The management of LAST is largely supportive. Immediate steps include stopping the administration of local anaesthetic, calling for help, providing 100% oxygen and securing the airway, establishing IV access, and controlling seizures with benzodiazepines or other medications. Cardiovascular status should be continuously assessed, and conventional therapies may be used to treat hypotension or arrhythmias. Intravenous lipid emulsion (intralipid) may also be considered as a treatment option.

If the patient goes into cardiac arrest, CPR should be initiated following ALS arrest algorithms, but lidocaine should not be used as an anti-arrhythmic therapy. Prolonged resuscitation may be necessary, and intravenous lipid emulsion should be administered. After the acute episode, the patient should be transferred to a clinical area with appropriate equipment and staff for further monitoring and care.

It is important to report cases of local anaesthetic toxicity to the appropriate authorities. Additionally, regular clinical review should be conducted to exclude pancreatitis, as intravenous lipid emulsion can interfere with amylase or lipase assays.

Activated charcoal is a commonly utilized substance for decontamination in cases of poisoning. Its main function is to attract and bind molecules of the ingested toxin onto its surface.

Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. This powder is created by subjecting carbonaceous matter to high heat, a process known as pyrolysis, and then concentrating it with a solution of zinc chloride. Through this process, the activated charcoal develops a complex network of pores, providing it with a large surface area of approximately 3,000 m2/g. This extensive surface area allows it to effectively hinder the absorption of the harmful toxin by up to 50%.

The typical dosage for adults is 50 grams, while children are usually given 1 gram per kilogram of body weight. Activated charcoal can be administered orally or through a nasogastric tube. It is crucial to administer it within one hour of ingestion, and if necessary, a second dose may be repeated after one hour.

Scleritis is a serious condition characterized by inflammation of the sclera, the white outer layer of the eye. It often affects both eyes, with bilateral involvement seen in about half of the cases. While the cause of scleritis can be unknown (idiopathic), it is associated with systemic inflammatory diseases like rheumatoid arthritis in approximately one-third of patients. In fact, scleritis can sometimes be the initial manifestation of these inflammatory conditions.

The clinical features of scleritis include moderate to severe pain, which can be felt in the brow or jaw. The pain worsens with eye movement and may disrupt sleep. The onset of symptoms is typically gradual. Other common symptoms include sensitivity to light (photophobia), excessive tearing (epiphora), and redness of both the superficial and deep episcleral vessels. The affected eye may also be tender to touch, and there may be a decrease in visual acuity. Some individuals may have a history of previous episodes of scleritis.

In summary, scleritis is a serious inflammatory disease of the sclera that can be associated with systemic inflammatory conditions. It presents with significant pain, often referred to the brow or jaw, and worsened by eye movement. Other symptoms include photophobia, excessive tearing, and redness of the episcleral vessels. It is important to recognize scleritis as it can be the first sign of underlying inflammatory diseases.

The diagnosis in this case is clearly gout. According to the guidelines from the European League Against Rheumatism (EULAR), 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 have effects on the bone marrow, leading to an increase in neutrophils and a decrease in platelets. Therefore, it should not be used in patients with blood disorders, as is the case with this patient.

Allopurinol should not be used during an acute gout attack 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.

Cluster headaches primarily affect men in their 20s, with a male to female ratio of 6:1. Smoking is also a contributing factor to the development of cluster headaches. These headaches typically occur in clusters, hence the name, lasting for a few weeks every year or two. The pain experienced is intense and localized, often felt around or behind the eye. It tends to occur at the same time each day and can lead to restlessness, with some patients resorting to hitting their head against a wall or the floor in an attempt to distract themselves from the pain.

In addition to the severe pain, cluster headaches also involve autonomic symptoms. These symptoms include redness and inflammation of the conjunctiva on the same side as the headache, as well as a runny nose and excessive tearing on the affected side. The pupil on the same side may also constrict, and there may be drooping of the eyelid on that side as well.

Overall, cluster headaches are a debilitating condition that predominantly affects young men. The pain experienced is excruciating and can lead to extreme measures to alleviate it. The associated autonomic symptoms further contribute to the discomfort and distress caused by these headaches.

Eosinophilic oesophagitis (EoE), also known as allergic inflammatory condition of the oesophagus, is characterized by the presence of eosinophils. It was identified as a clinical condition about two decades ago but has gained recognition more recently. EoE is most commonly observed in middle-aged individuals, with an average age of diagnosis ranging from 30 to 50 years. It is more prevalent in men, with a male-to-female ratio of 3:1. Allergic conditions, particularly atopy, are often associated with EoE.

The clinical manifestations of EoE vary depending on the age of the patient. In adults, common symptoms include dysphagia, food bolus obstruction, heartburn, and chest pain. On the other hand, children with EoE may present with failure to thrive, food refusal, difficulty feeding, vomiting, and abdominal pain.

To diagnose EoE, it is crucial to consider the possibility of this condition in patients who have persistent heartburn and/or difficulty swallowing, especially if they have a history of allergies or atopic disease. Diagnosis is confirmed by identifying more than 15 eosinophils per high-power field on an oesophageal biopsy. Allergy testing is not effective as EoE is not mediated by IgE.

There are three main management options for EoE, all of which are considered first-line treatments. The first option is proton pump inhibitors (PPIs), which are effective in approximately one-third of patients. If an endoscopic biopsy confirms the presence of eosinophils, an 8-week trial of PPIs can be initiated. After the trial, a repeat endoscopy and biopsy should be performed to assess for persistent eosinophils. Patients who respond to PPIs are diagnosed with PPI responsive oesophageal eosinophilia, while those who do not respond are diagnosed with true eosinophilic oesophagitis.

The second management option is dietary manipulation, which can be effective in both children and adults. It can be used as an initial treatment or in combination with pharmacological therapy. The six most commonly implicated food groups in EoE are cow’s milk, wheat, egg, soy, peanut/tree nut, and fish/shellfish. There are four main approaches to dietary manipulation: elemental diet, six food elimination diet (SFED), four food elimination diet (FFED),

Hypercalcaemia, which is an elevated level of calcium in the blood, is most commonly caused by primary hyperparathyroidism and malignancy in the UK. However, there are other factors that can contribute to hypercalcaemia as well. These include an increase in dietary intake of calcium, excessive intake of vitamin D, tertiary hyperparathyroidism, overactive thyroid gland (hyperthyroidism), Addison’s disease, sarcoidosis, Paget’s disease, multiple myeloma, phaeochromocytoma, and milk-alkali syndrome. Additionally, certain medications such as lithium, thiazide diuretics, and theophyllines can also lead to hypercalcaemia. It is important to be aware of these various causes in order to properly diagnose and treat this condition.

Generalized anxiety disorder (GAD) is the most probable diagnosis in this case.

The primary distinction between GAD and panic disorder lies in their symptoms. GAD is primarily characterized by anxiety, whereas panic disorder is characterized by panic attacks. Individuals with GAD typically do not experience frequent panic attacks, although they may occasionally occur. In this patient’s case, while he did experience occasional panic attacks, they were not his main symptom, and his anxiety was not centered around these episodes.

GAD is associated with persistent physical symptoms such as muscle tension, aches, headaches, fatigue, trembling, twitching, irritability, difficulty swallowing, and the sensation of a lump in the throat.

On the other hand, panic disorder primarily revolves around the panic attacks themselves. A panic attack is a brief and intense episode characterized by overwhelming feelings of dread and fear, which may or may not be triggered by a specific situation. Common physical symptoms experienced during panic attacks include dizziness, sweating, chills, nausea, trembling, shaking, abdominal cramps, throat tightness, shortness of breath, numbness in the extremities, rapid heartbeat, palpitations, and chest pain.