ATLS guidelines now suggest administering only 1 liter of crystalloid fluid during the initial assessment. If patients do not respond to the crystalloid, it is recommended to quickly transition to blood products. Studies have shown that infusing more than 1.5 liters of crystalloid fluid is associated with higher mortality rates in trauma cases. Therefore, it is advised to prioritize the early use of blood products and avoid large volumes of crystalloid fluid in trauma patients. In cases where it is necessary, massive transfusion should be considered, defined as the transfusion of more than 10 units of blood in 24 hours or more than 4 units of blood in one hour. For patients with evidence of Class III and IV hemorrhage, early resuscitation with blood and blood products in low ratios is recommended.

Based on the findings of significant trials, such as the CRASH-2 study, the use of tranexamic acid is now recommended within 3 hours. This involves administering a loading dose of 1 gram intravenously over 10 minutes, followed by an infusion of 1 gram over eight hours. In some regions, tranexamic acid is also being utilized in the prehospital setting.

Haloperidol, when administered during the third trimester of pregnancy, can lead to extrapyramidal symptoms in the newborn. These symptoms may include agitation, poor feeding, excessive sleepiness, and difficulty breathing. The severity of these side effects can vary, with some infants requiring intensive care and extended hospital stays. It is important to closely monitor exposed neonates for signs of extrapyramidal syndrome or withdrawal. Haloperidol should only be used during pregnancy if the benefits clearly outweigh the risks to the fetus.

Below is a list outlining commonly encountered drugs that have adverse effects during pregnancy:

ACE inhibitors (e.g. ramipril): If given during the second and third trimesters, these drugs can cause hypoperfusion, renal failure, and the oligohydramnios sequence.

Aminoglycosides (e.g. gentamicin): These drugs can cause ototoxicity and deafness in the fetus.

Aspirin: High doses of aspirin can lead to first-trimester abortions, delayed onset of labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g. 75 mg) do not pose significant risks.

Benzodiazepines (e.g. diazepam): When administered late in pregnancy, these drugs can cause respiratory depression and a neonatal withdrawal syndrome.

Calcium-channel blockers: If given during the first trimester, these drugs can cause phalangeal abnormalities. If given during the second and third trimesters, they can result in fetal growth retardation.

Carbamazepine: This drug can lead to hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol: Administration of chloramphenicol can cause gray baby syndrome in newborns.

Corticosteroids: If given during the first trimester, corticosteroids may cause orofacial clefts in the fetus.

Danazol: When administered during the first trimester, danazol can cause masculinization of the female fetuses genitals.

Finasteride: Pregnant women should avoid handling finasteride as crushed or broken tablets can be absorbed through the skin and affect male sex organ development.

Haloperidol: If given during the first trimester, haloperidol may cause limb malformations. If given during the third trimester, there is an increased risk of extrapyramidal symptoms in the neonate.

Pabrinex is a supplement that includes a combination of essential vitamins. These vitamins are Thiamine (also known as vitamin B1), Riboflavin (commonly referred to as vitamin B2), Nicotinamide (which encompasses Vitamin B3, niacin, and nicotinic acid), Pyridoxine (known as vitamin B6), and Ascorbic acid (which is vitamin C). Each of these vitamins plays a crucial role in maintaining our overall health and well-being. By incorporating Pabrinex into our daily routine, we can ensure that our bodies receive the necessary nutrients to support various bodily functions.

Malaria is a contagious illness that is spread by female mosquitoes of the Anopheles genus. It is caused by a parasitic infection from the Plasmodium genus. There are five species of Plasmodium that can cause disease in humans: Plasmodium falciparum, Plasmodium ovale, Plasmodium vivax, Plasmodium malariae, and Plasmodium knowlesi.

The main symptom of malaria is the malarial paroxysm, which is a recurring cycle of cold, hot, and sweating stages. During the cold stage, the patient experiences intense chills, followed by an extremely hot stage, and finally a stage of profuse sweating. Upon examination, the patient may show signs of anemia, jaundice, and have an enlarged liver and spleen, but no signs of swollen lymph nodes.

Plasmodium falciparum is the most severe form of malaria and is responsible for the majority of deaths. Severe or complicated malaria is indicated by impaired consciousness, seizures, low blood sugar, anemia, kidney damage, difficulty breathing, and spontaneous bleeding. Given the presentation, it is likely that this case involves Plasmodium falciparum.

Currently, artemisinin-based combination therapy (ACT) is recommended for treating P. falciparum malaria. This involves combining fast-acting artemisinin-based compounds with a drug from a different class. Companion drugs include lumefantrine, mefloquine, amodiaquine, sulfadoxine/pyrimethamine, piperaquine, and chlorproguanil/dapsone. Artemisinin derivatives include dihydroartemisinin, artesunate, and artemether.

If ACT is not available, oral quinine or atovaquone with proguanil hydrochloride can be used. Quinine is highly effective but not well tolerated for long-term treatment, so it should be combined with another drug, usually oral doxycycline (or clindamycin for pregnant women and young children).

Severe or complicated falciparum malaria should be managed in a high dependency unit or intensive care setting. Intravenous artesunate is recommended for all patients with severe or complicated falciparum malaria, or those at high risk of developing severe disease (such as if more than 2% of red blood cells are infected), or

The septum, which is a part of the heart, can be best identified by examining leads V1 and V2. The septum receives its blood supply from the proximal left anterior descending artery (LAD). The LAD is responsible for supplying blood to the anterior myocardium and also contributes to the blood supply of the lateral myocardium. If the LAD becomes blocked, it can result in ST elevation in all the chest leads.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

Hyperosmolar hyperglycaemic state (HHS) is a condition characterized by extremely high blood sugar levels, dehydration, and increased osmolality without significant ketosis. In this patient, the symptoms are consistent with HHS as they have high blood sugar levels without significant ketoacidosis (pH is above 7.3 and ketones are less than 3 mmol/L). Additionally, they show signs of dehydration with low blood pressure and a fast heart rate. The osmolality is calculated to be equal to or greater than 320 mosmol/kg, indicating increased concentration of solutes in the blood.

Further Reading:

Hyperosmolar hyperglycaemic state (HHS) is a syndrome that occurs in people with type 2 diabetes and is characterized by extremely high blood glucose levels, dehydration, and hyperosmolarity without significant ketosis. It can develop over days or weeks and has a mortality rate of 5-20%, which is higher than that of diabetic ketoacidosis (DKA). HHS is often precipitated by factors such as infection, inadequate diabetic treatment, physiological stress, or certain medications.

Clinical features of HHS include polyuria, polydipsia, nausea, signs of dehydration (hypotension, tachycardia, poor skin turgor), lethargy, confusion, and weakness. Initial investigations for HHS include measuring capillary blood glucose, venous blood gas, urinalysis, and an ECG to assess for any potential complications such as myocardial infarction. Osmolality should also be calculated to monitor the severity of the condition.

The management of HHS aims to correct dehydration, hyperglycaemia, hyperosmolarity, and electrolyte disturbances, as well as identify and treat any underlying causes. Intravenous 0.9% sodium chloride solution is the principal fluid used to restore circulating volume and reverse dehydration. If the osmolality does not decline despite adequate fluid balance, a switch to 0.45% sodium chloride solution may be considered. Care must be taken in correcting plasma sodium and osmolality to avoid complications such as cerebral edema and osmotic demyelination syndrome.

The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours, and the fall in blood glucose should be no more than 5 mmol/L per hour. Low-dose intravenous insulin may be initiated if the blood glucose is not falling with fluids alone or if there is significant ketonaemia. Potassium replacement should be guided by the potassium level, and the patient should be encouraged to drink as soon as it is safe to do so.

Complications of treatment, such as fluid overload, cerebral edema, or central pontine myelinolysis, should be assessed for, and underlying precipitating factors should be identified and treated. Prophylactic anticoagulation is required in most patients, and all patients should be assumed to be at high risk of foot ulceration, necessitating appropriate foot protection and daily foot checks.

Testicular torsion is the correct diagnosis in this case. When a patient presents with sudden, severe, and acute testicular pain, testicular torsion should be assumed until proven otherwise. There are several historical factors that support this diagnosis. These include the pain occurring suddenly, being accompanied by vomiting, happening during sleep (as half of torsions occur during sleep), a previous history of torsion in the other testis, previous episodes that have resolved recently, and a history of undescended testis.

On examination, there are certain findings that further suggest testicular torsion. The testis may be positioned high in the scrotum and too tender to touch. The opposite testis may lie horizontally (known as Angell’s sign). Pain is not relieved by elevating the testis (negative Prehn’s sign), and the cremasteric reflex may be absent.

It is important to recognize that testicular torsion is a surgical emergency that requires immediate assessment and intervention to restore blood flow. Irreversible damage can occur within six hours of onset, so prompt treatment is crucial in this patient.

The first-line treatment for Addisonian (adrenal) crisis is hydrocortisone. This patient displays symptoms that indicate an Addisonian crisis, and the main components of their management involve administering hydrocortisone and providing intravenous fluids for resuscitation.

Further Reading:

Addison’s disease, also known as primary adrenal insufficiency or hypoadrenalism, is a rare disorder caused by the destruction of the adrenal cortex. This leads to reduced production of glucocorticoids, mineralocorticoids, and adrenal androgens. The deficiency of cortisol results in increased production of adrenocorticotropic hormone (ACTH) due to reduced negative feedback to the pituitary gland. This condition can cause metabolic disturbances such as hyperkalemia, hyponatremia, hypercalcemia, and hypoglycemia.

The symptoms of Addison’s disease can vary but commonly include fatigue, weight loss, muscle weakness, and low blood pressure. It is more common in women and typically affects individuals between the ages of 30-50. The most common cause of primary hypoadrenalism in developed countries is autoimmune destruction of the adrenal glands. Other causes include tuberculosis, adrenal metastases, meningococcal septicaemia, HIV, and genetic disorders.

The diagnosis of Addison’s disease is often suspected based on low cortisol levels and electrolyte abnormalities. The adrenocorticotropic hormone stimulation test is commonly used for confirmation. Other investigations may include adrenal autoantibodies, imaging scans, and genetic screening.

Addisonian crisis is a potentially life-threatening condition that occurs when there is an acute deficiency of cortisol and aldosterone. It can be the first presentation of undiagnosed Addison’s disease. Precipitating factors of an Addisonian crisis include infection, dehydration, surgery, trauma, physiological stress, pregnancy, hypoglycemia, and acute withdrawal of long-term steroids. Symptoms of an Addisonian crisis include malaise, fatigue, nausea or vomiting, abdominal pain, fever, muscle pains, dehydration, confusion, and loss of consciousness.

There is no fixed consensus on diagnostic criteria for an Addisonian crisis, as symptoms are non-specific. Investigations may include blood tests, blood gas analysis, and septic screens if infection is suspected. Management involves administering hydrocortisone and fluids. Hydrocortisone is given parenterally, and the dosage varies depending on the age of the patient. Fluid resuscitation with saline is necessary to correct any electrolyte disturbances and maintain blood pressure. The underlying cause of the crisis should also be identified and treated. Close monitoring of sodium levels is important to prevent complications such as osmotic demyelination syndrome.

Tenecteplase is a medication known as a tissue plasminogen activator (tPA). Its main mechanism of action involves binding specifically to fibrin and converting plasminogen into plasmin. This process leads to the breakdown of the fibrin matrix and promotes reperfusion at the affected site. Among the options provided, Tenecteplase is the sole drug that primarily acts by facilitating reperfusion.

Acute mastoiditis commonly occurs as a complication of acute otitis media (AOM). In this case, the patient exhibits symptoms indicative of acute mastoiditis. The infection typically spreads from the middle ear tympanic cavity (acute otitis media) to the mastoid antrum through a narrow canal within the petrous temporal bone.

Further Reading:

Mastoiditis is an infection of the mastoid air cells, which are located in the mastoid process of the skull. It is usually caused by the spread of infection from the middle ear. The most common organism responsible for mastoiditis is Streptococcus pneumoniae, but other bacteria and fungi can also be involved. The infection can spread to surrounding structures, such as the meninges, causing serious complications like meningitis or cerebral abscess.

Mastoiditis can be classified as acute or chronic. Acute mastoiditis is a rare complication of acute otitis media, which is inflammation of the middle ear. It is characterized by severe ear pain, fever, swelling and redness behind the ear, and conductive deafness. Chronic mastoiditis is usually associated with chronic suppurative otitis media or cholesteatoma and presents with recurrent episodes of ear pain, headache, and fever.

Mastoiditis is more common in children, particularly those between 6 and 13 months of age. Other risk factors include immunocompromised patients, those with intellectual impairment or communication difficulties, and individuals with cholesteatoma.

Diagnosis of mastoiditis involves a physical examination, blood tests, ear swab for culture and sensitivities, and imaging studies like contrast-enhanced CT or MRI. Treatment typically involves referral to an ear, nose, and throat specialist, broad-spectrum intravenous antibiotics, pain relief, and myringotomy (a procedure to drain fluid from the middle ear).

Complications of mastoiditis are rare but can be serious. They include intracranial abscess, meningitis, subperiosteal abscess, neck abscess, venous sinus thrombosis, cranial nerve palsies, hearing loss, labyrinthitis, extension to the zygoma, and carotid artery arteritis. However, most patients with mastoiditis have a good prognosis and do not experience long-term ear problems.

A pH level in the arteries that is below 7.30 on or after the second day following a paracetamol overdose is considered a poor indicator of prognosis. Additionally, a prolonged prothrombin time (PT) of over 100 seconds (indicated by an international normalized ratio (INR) of over 6.5), along with a high plasma creatinine level of over 300 μmol/L and grade 3 or 4 hepatic encephalopathy, are also poor prognostic indicators and may indicate the need for a liver transplant. Furthermore, an increase in PT between the third and fourth day after the overdose is also considered a poor prognostic indicator.

Further Reading:

Paracetamol poisoning occurs when the liver is unable to metabolize paracetamol properly, leading to the production of a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI). Normally, NAPQI is conjugated by glutathione into a non-toxic form. However, during an overdose, the liver’s conjugation systems become overwhelmed, resulting in increased production of NAPQI and depletion of glutathione stores. This leads to the formation of covalent bonds between NAPQI and cell proteins, causing cell death in the liver and kidneys.

Symptoms of paracetamol poisoning may not appear for the first 24 hours or may include abdominal symptoms such as nausea and vomiting. After 24 hours, hepatic necrosis may develop, leading to elevated liver enzymes, right upper quadrant pain, and jaundice. Other complications can include encephalopathy, oliguria, hypoglycemia, renal failure, and lactic acidosis.

The management of paracetamol overdose depends on the timing and amount of ingestion. Activated charcoal may be given if the patient presents within 1 hour of ingesting a significant amount of paracetamol. N-acetylcysteine (NAC) is used to increase hepatic glutathione production and is given to patients who meet specific criteria. Blood tests are taken to assess paracetamol levels, liver function, and other parameters. Referral to a medical or liver unit may be necessary, and psychiatric follow-up should be considered for deliberate overdoses.

In cases of staggered ingestion, all patients should be treated with NAC without delay. Blood tests are also taken, and if certain criteria are met, NAC can be discontinued. Adverse reactions to NAC are common and may include anaphylactoid reactions, rash, hypotension, and nausea. Treatment for adverse reactions involves medications such as chlorpheniramine and salbutamol, and the infusion may be stopped if necessary.

The prognosis for paracetamol poisoning can be poor, especially in cases of severe liver injury. Fulminant liver failure may occur, and liver transplant may be necessary. Poor prognostic indicators include low arterial pH, prolonged prothrombin time, high plasma creatinine, and hepatic encephalopathy.

During the first trimester of pregnancy, the use of warfarin can lead to a condition known as fetal warfarin syndrome. This condition is characterized by nasal hypoplasia, bone stippling, bilateral optic atrophy, and intellectual disability in the baby. However, if warfarin is taken during the second or third trimester, it can cause optic atrophy, cataracts, microcephaly, microphthalmia, intellectual disability, and both fetal and maternal hemorrhage.

There are several other drugs that can have adverse effects during pregnancy. For example, ACE inhibitors like ramipril can cause hypoperfusion, renal failure, and the oligohydramnios sequence if taken during the second and third trimesters. Aminoglycosides such as gentamicin can lead to ototoxicity and deafness in the baby. High doses of aspirin can result in first trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses of aspirin (e.g. 75 mg) do not pose significant risks.

Benzodiazepines like diazepam, when taken late in pregnancy, can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if taken during the first trimester, can cause phalangeal abnormalities, while their use in the second and third trimesters can lead to fetal growth retardation. Carbamazepine can result in hemorrhagic disease of the newborn and neural tube defects. Chloramphenicol can cause gray baby syndrome. Corticosteroids, if taken during the first trimester, may cause orofacial clefts.

Danazol, if taken during the first trimester, can cause masculinization of the female fetuses genitals. Finasteride should not be handled by pregnant women as crushed or broken tablets can be absorbed through the skin and affect male sex organ development. Haloperidol, if taken during the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the newborn.

Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the baby. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations and spontaneous abortion.

The symptoms of acute mountain sickness (AMS) typically appear within 6-12 hours of reaching an altitude above 2500 meters. On the other hand, the onset of high altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE) usually occurs after 2-4 days of being at high altitude.

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.

A needle cricothyroidotomy is a procedure used in emergency situations to provide oxygenation when intubation and oxygenation are not possible. It is typically performed when a patient cannot be intubated or oxygenated. There are certain conditions that make this procedure contraindicated, such as local infection, distorted anatomy, previous failed attempts, and swelling or mass lesions.

To perform a needle cricothyroidotomy, the necessary equipment should be assembled and prepared. The patient should be positioned supine with their neck in a neutral position. The neck should be cleaned in a sterile manner using antiseptic swabs. If time allows, the area should be anesthetized locally. A 12 or 14 gauge over-the-needle catheter should be assembled to a 10 mL syringe.

The cricothyroid membrane, located between the thyroid and cricoid cartilage, should be identified anteriorly. The trachea should be stabilized with the thumb and forefinger of one hand. Using the other hand, the skin should be punctured in the midline with the needle over the cricothyroid membrane. The needle should be directed at a 45° angle caudally while negative pressure is applied to the syringe. Needle aspiration should be maintained as the needle is inserted through the lower half of the cricothyroid membrane, with air aspiration indicating entry into the tracheal lumen.

Once the needle is in place, the syringe and needle should be removed while the catheter is advanced to the hub. The oxygen catheter should be attached and the airway secured. It is important to be aware of possible complications, such as technique failure, cannula obstruction or dislodgement, injury to local structures, and surgical emphysema if high flow oxygen is administered through a malpositioned cannula.

Blood transfusion is a potentially life-saving treatment that can provide great clinical benefits. However, it also carries several risks and potential problems. These include immunological complications, administration errors, infections, immune dilution, and transfusion errors. While there have been improvements in safety procedures and efforts to minimize the use of transfusion, errors and serious adverse reactions still occur and often go unreported.

One rare complication of blood transfusion is transfusion-associated graft-vs-host disease (TA-GVHD). This condition typically presents with fever, rash, and diarrhea 1-4 weeks after the transfusion. Laboratory findings may show pancytopenia and abnormalities in liver function. Unlike GVHD after marrow transplantation, TA-GVHD leads to severe marrow aplasia with a mortality rate exceeding 90%. Unfortunately, there are currently no effective treatments available for this condition, and survival is rare, with death usually occurring within 1-3 weeks of the first symptoms.

During a blood transfusion, viable T lymphocytes from the donor are transfused into the recipient’s body. In TA-GVHD, these lymphocytes engraft and react against the recipient’s tissues. However, the recipient is unable to reject the donor lymphocytes due to factors such as immunodeficiency, severe immunosuppression, or shared HLA antigens. Supportive management is the only option for TA-GVHD.

The following summarizes the main complications and reactions that can occur during a blood transfusion:

Complication Features Management
Febrile transfusion reaction
– Presents with a 1-degree rise in temperature from baseline, along with chills and malaise.
– Most common reaction, occurring in 1 out of 8 transfusions.
– Usually caused by cytokines from leukocytes in transfused red cell or platelet components.
– Supportive management, with the use of paracetamol for symptom relief.

Acute haemolytic reaction
– Symptoms include fever, chills, pain at the transfusion site, nausea, vomiting, and dark urine.
– Often accompanied by a feeling of ‘impending doom’.
– Most serious type of reaction, often due to ABO incompatibility caused by administration errors.
– Immediate action required: stop the transfusion, administer IV fluids, and consider diuretics if necessary.

Delayed haemolytic reaction
– Typically occurs 4-8 days after a blood transfusion.
– Symptoms include fever, anemia and/or hyperbilirubinemia

This patient is experiencing hyponatremia, which is characterized by low plasma osmolality and high urine osmolality, indicating syndrome of inappropriate antidiuretic hormone secretion (SIADH). One of the most common causes of SIADH is the use of SSRIs. On the other hand, lithium, sodium bicarbonate, and corticosteroids are known to cause hypernatremia. Plasma osmolality can be calculated using the formula (2 x Na) + Glucose + Urea. In this patient, the calculated osmolality is 265 mosmol/kg, which falls within the normal range of 275-295 mosmol/kg.

Further Reading:

Syndrome of inappropriate antidiuretic hormone (SIADH) is a condition characterized by low sodium levels in the blood due to excessive secretion of antidiuretic hormone (ADH). ADH, also known as arginine vasopressin (AVP), is responsible for promoting water and sodium reabsorption in the body. SIADH occurs when there is impaired free water excretion, leading to euvolemic (normal fluid volume) hypotonic hyponatremia.

There are various causes of SIADH, including malignancies such as small cell lung cancer, stomach cancer, and prostate cancer, as well as neurological conditions like stroke, subarachnoid hemorrhage, and meningitis. Infections such as tuberculosis and pneumonia, as well as certain medications like thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs), can also contribute to SIADH.

The diagnostic features of SIADH include low plasma osmolality, inappropriately elevated urine osmolality, urinary sodium levels above 30 mmol/L, and euvolemic. Symptoms of hyponatremia, which is a common consequence of SIADH, include nausea, vomiting, headache, confusion, lethargy, muscle weakness, seizures, and coma.

Management of SIADH involves correcting hyponatremia slowly to avoid complications such as central pontine myelinolysis. The underlying cause of SIADH should be treated if possible, such as discontinuing causative medications. Fluid restriction is typically recommended, with a daily limit of around 1000 ml for adults. In severe cases with neurological symptoms, intravenous hypertonic saline may be used. Medications like demeclocycline, which blocks ADH receptors, or ADH receptor antagonists like tolvaptan may also be considered.

It is important to monitor serum sodium levels closely during treatment, especially if using hypertonic saline, to prevent rapid correction that can lead to central pontine myelinolysis. Osmolality abnormalities can help determine the underlying cause of hyponatremia, with increased urine osmolality indicating dehydration or renal disease, and decreased urine osmolality suggesting SIADH or overhydration.

Extrapyramidal side effects refer to drug-induced movements that encompass acute dyskinesias and dystonic reactions, tardive dyskinesia, Parkinsonism, akinesia, akathisia, and neuroleptic malignant syndrome. These side effects occur due to the blockade or depletion of dopamine in the basal ganglia, leading to a lack of dopamine that often resembles idiopathic disorders of the extrapyramidal system.

The primary culprits behind extrapyramidal side effects are the first-generation antipsychotics, which act as potent antagonists of the dopamine D2 receptor. Among these antipsychotics, haloperidol and fluphenazine are the two drugs most commonly associated with extrapyramidal side effects. On the other hand, second-generation antipsychotics like olanzapine have lower rates of adverse effects on the extrapyramidal system compared to their first-generation counterparts.

While less frequently, other medications can also contribute to extrapyramidal symptoms. These include certain antidepressants, lithium, various anticonvulsants, antiemetics, and, in rare cases, oral contraceptive agents.

When the INR (International Normalized Ratio) is above 8 but there is no sign of bleeding, the usual approach is to stop administering warfarin and instead provide oral vitamin K. If the INR is below 8 and there is no evidence of bleeding, it is appropriate to discontinue warfarin. However, if there is evidence of bleeding or the INR exceeds 8, reversal agents are administered. In cases where the INR is greater than 8 without any bleeding, oral vitamin K is typically prescribed at a dosage of 1-5 mg.

Further Reading:

Management of High INR with Warfarin

Major Bleeding:
– Stop warfarin immediately.
– Administer intravenous vitamin K 5 mg.
– Administer 25-50 u/kg four-factor prothrombin complex concentrate.
– If prothrombin complex concentrate is not available, consider using fresh frozen plasma (FFP).
– Seek medical attention promptly.

INR > 8.0 with Minor Bleeding:
– Stop warfarin immediately.
– Administer intravenous vitamin K 1-3mg.
– Repeat vitamin K dose if INR remains high after 24 hours.
– Restart warfarin when INR is below 5.0.
– Seek medical advice if bleeding worsens or persists.

INR > 8.0 without Bleeding:
– Stop warfarin immediately.
– Administer oral vitamin K 1-5 mg using the intravenous preparation orally.
– Repeat vitamin K dose if INR remains high after 24 hours.
– Restart warfarin when INR is below 5.0.
– Seek medical advice if any symptoms or concerns arise.

INR 5.0-8.0 with Minor Bleeding:
– Stop warfarin immediately.
– Administer intravenous vitamin K 1-3mg.
– Restart warfarin when INR is below 5.0.
– Seek medical advice if bleeding worsens or persists.

INR 5.0-8.0 without Bleeding:
– Withhold 1 or 2 doses of warfarin.
– Reduce subsequent maintenance dose.
– Monitor INR closely and seek medical advice if any concerns arise.

Note: In cases of intracranial hemorrhage, prothrombin complex concentrate should be considered as it is faster acting than fresh frozen plasma (FFP).

The BTS guidelines for managing acute asthma in adults provide the following recommendations:

Oxygen:
– It is important to give supplementary oxygen to all patients with acute severe asthma who have low levels of oxygen in their blood (hypoxemia). The goal is to maintain a blood oxygen saturation level (SpO2) between 94-98%. Even if pulse oximetry is not available, oxygen should still be administered.

β2 agonists therapy:
– High-dose inhaled β2 agonists should be used as the first-line treatment for patients with acute asthma. It is important to administer these medications as early as possible.
– Intravenous β2 agonists should be reserved for patients who cannot reliably use inhaled therapy.
– For patients with life-threatening asthma symptoms, nebulized β2 agonists driven by oxygen are recommended.
– In cases of severe asthma that does not respond well to an initial dose of β2 agonist, continuous nebulization with an appropriate nebulizer may be considered.

Ipratropium bromide:
– Nebulized ipratropium bromide (0.5 mg every 4-6 hours) should be added to β2 agonist treatment for patients with acute severe or life-threatening asthma, or those who do not respond well to initial β2 agonist therapy.

Steroid therapy:
– Steroids should be given in adequate doses for all cases of acute asthma attacks.
– Prednisolone should be continued at a dose of 40-50 mg daily for at least five days or until the patient recovers.

Other therapies:
– Nebulized magnesium is not recommended for the treatment of acute asthma in adults.
– A single dose of intravenous magnesium sulfate may be considered for patients with acute severe asthma (peak expiratory flow rate <50% of the best or predicted value) who do not respond well to inhaled bronchodilator therapy. However, this should only be done after consulting with senior medical staff.
– Routine prescription of antibiotics is not necessary for patients with acute asthma.

For more information, please refer to the BTS/SIGN Guideline on the Management of Asthma.

There are two scoring systems that NICE recommends for assessing sore throat: the Centor Clinical Prediction Score and the FeverPAIN Score.

The Centor Clinical Prediction Score was initially developed as a tool to determine the likelihood of a group A beta-haemolytic Streptococcus (GABHS) infection in adults with a sore throat. This score was created and tested in US Emergency Departments, specifically for adult patients.

The Centor score evaluates patients based on several criteria, with one point given for each positive criterion. These criteria include a history of fever (temperature above 38°C), the presence of exudate or swelling on the tonsils, tender or swollen anterior cervical lymph nodes, and the absence of cough.

According to the current NICE guidance, the Centor score can be used to guide management in the following way:
– A score of 0 to 2 indicates a 3-17% likelihood of streptococcus isolation, and antibiotics are not recommended.
– A score of 3 to 4 indicates a 32-56% likelihood of streptococcus isolation, and immediate treatment with empirical antibiotics or a backup prescription should be considered.

By utilizing these scoring systems, healthcare professionals can make more informed decisions regarding the management and treatment of patients with sore throat.

Sexually transmitted eye infections can be quite severe and are often characterized by prolonged mucopurulent discharge. There are two main causes of these infections: Chlamydia trachomatis and Neisseria gonorrhoea. Differentiating between the two can be done by considering certain features.

Chlamydia trachomatis infection typically presents with chronic low-grade irritation and mucous discharge that lasts for more than two weeks in sexually active individuals. It may also be accompanied by pre-auricular lymphadenopathy. This type of infection is usually unilateral but can sometimes affect both eyes.

On the other hand, Neisseria gonorrhoea infection tends to develop rapidly, usually within 12 to 24 hours. It is characterized by copious mucopurulent discharge, eyelid swelling, and tender preauricular lymphadenopathy. This type of infection carries a higher risk of complications, such as uveitis, severe keratitis, and corneal perforation.

Based on the patient’s symptoms, it appears that they are more consistent with a Neisseria gonorrhoea infection. The rapid onset, copious discharge, and tender preauricular lymphadenopathy are indicative of this type of infection.

Treatment for gonococcal conjunctivitis in adults is typically based on limited research. However, a study has shown that all 12 patients responded well to a single 1 g intramuscular injection of ceftriaxone, along with a single episode of ocular lavage with saline.

In summary, sexually transmitted eye infections can be caused by either Chlamydia trachomatis or Neisseria gonorrhoea. Differentiating between the two is important in order to provide appropriate treatment. The patient in this case exhibits symptoms that align more closely with a Neisseria gonorrhoea infection, which carries a higher risk of complications. Treatment options for gonococcal conjunctivitis are limited, but a single injection of ceftriaxone has shown positive results in previous studies.

During the third trimester of pregnancy, the use of selective serotonin reuptake inhibitors (SSRIs) has been associated with a discontinuation syndrome and persistent pulmonary hypertension of the newborn. It is important to be aware of the adverse effects of various drugs during pregnancy. For example, ACE inhibitors like ramipril, if given in the second and third trimester, can cause hypoperfusion, renal failure, and the oligohydramnios sequence. Aminoglycosides such as gentamicin can lead to ototoxicity and deafness. High doses of aspirin can result in first-trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g., 75 mg) do not pose significant risks. Late administration of benzodiazepines like diazepam during pregnancy can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if given in the first trimester, may cause phalangeal abnormalities, while their use in the second and third trimester can lead to fetal growth retardation. Carbamazepine has been associated with hemorrhagic disease of the newborn and neural tube defects. Chloramphenicol can cause grey baby syndrome. Corticosteroids, if given in the first trimester, may cause orofacial clefts. Danazol, if administered in the first trimester, can result in masculinization of the female fetuses genitals. Pregnant women should avoid handling crushed or broken tablets of finasteride as it can be absorbed through the skin and affect male sex organ development. Haloperidol, if given in the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the neonate. Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability. The use of lithium in the first trimester increases the risk of fetal cardiac malformations, while its use in the second and third trimesters can result in hypotonia, lethargy, feeding problems, hypothyroidism, goiter, and nephrogenic diabetes insipidus.

Corticosteroids are the primary treatment for croup. In this case, the child’s symptoms align with croup. The recommended initial medication for croup is a one-time oral dose of dexamethasone, regardless of the severity of the condition. The dosage is typically 0.15mg per kilogram of the child’s weight.

Further Reading:

Croup, also known as laryngotracheobronchitis, is a respiratory infection that primarily affects infants and toddlers. It is characterized by a barking cough and can cause stridor (a high-pitched sound during breathing) and respiratory distress due to swelling of the larynx and excessive secretions. The majority of cases are caused by parainfluenza viruses 1 and 3. Croup is most common in children between 6 months and 3 years of age and tends to occur more frequently in the autumn.

The clinical features of croup include a barking cough that is worse at night, preceded by symptoms of an upper respiratory tract infection such as cough, runny nose, and congestion. Stridor, respiratory distress, and fever may also be present. The severity of croup can be graded using the NICE system, which categorizes it as mild, moderate, severe, or impending respiratory failure based on the presence of symptoms such as cough, stridor, sternal/intercostal recession, agitation, lethargy, and decreased level of consciousness. The Westley croup score is another commonly used tool to assess the severity of croup based on the presence of stridor, retractions, air entry, oxygen saturation levels, and level of consciousness.

In cases of severe croup with significant airway obstruction and impending respiratory failure, symptoms may include a minimal barking cough, harder-to-hear stridor, chest wall recession, fatigue, pallor or cyanosis, decreased level of consciousness, and tachycardia. A respiratory rate over 70 breaths per minute is also indicative of severe respiratory distress.

Children with moderate or severe croup, as well as those with certain risk factors such as chronic lung disease, congenital heart disease, neuromuscular disorders, immunodeficiency, age under 3 months, inadequate fluid intake, concerns about care at home, or high fever or a toxic appearance, should be admitted to the hospital. The mainstay of treatment for croup is corticosteroids, which are typically given orally. If the child is too unwell to take oral medication, inhaled budesonide or intramuscular dexamethasone may be used as alternatives. Severe cases may require high-flow oxygen and nebulized adrenaline.

When considering the differential diagnosis for acute stridor and breathing difficulty, non-infective causes such as inhaled foreign bodies.

In patients who have undergone tonsillectomy and are experiencing severe bleeding, it is recommended to apply either Co-phenylcaine spray (a combination of lidocaine and phenylephrine) or 1:10,000 adrenaline soaked gauze/dental roll to the bleeding points. This helps to constrict the blood vessels and slow down the bleeding rate.

To apply topical adrenaline, a dental roll or gauze soaked in 1:10,000 adrenaline solution is used. It is applied to the bleeding point using Magill’s forceps, with pressure directed laterally (not posteriorly). However, this may not be possible if the patient has a strong gag reflex. To minimize the risk of inhalation and facilitate suction, the patient’s head should be tilted to the side and/or forwards.

For light or intermittent bleeding, hydrogen peroxide gargles can be used. However, they are not recommended for heavy bleeds.

Further Reading:

Tonsillectomy is a common procedure performed by ENT surgeons in the UK, with over 50,000 surgeries performed each year. While it is considered routine, there are risks of serious complications, including post-tonsillectomy bleeding. Approximately 5% of patients experience bleeding after the procedure, with most cases being self-limiting. However, severe bleeding can lead to hypovolemia and airway obstruction from clots, which can be life-threatening.

Post-tonsillectomy bleeding can be classified as primary (reactive) or secondary (delayed). Primary bleeding occurs within 24 hours of the procedure, while secondary bleeding occurs more than 24 hours post-procedure. Secondary bleeding is often caused by factors such as sloughing of eschar, trauma from solid food ingestion, tonsil bed infection, postoperative NSAID usage, or unknown causes.

Patients may present with symptoms such as vomiting blood, coughing up blood, tasting blood in the throat, finding blood on pillows or bed sheets, or excessive swallowing (especially in children). It is important for clinicians to assess the severity of blood loss, although it can be challenging to accurately estimate in children.

The ABCDE approach should be used to assess patients, with a focus on airway compromise, hemodynamic instability, and evidence of bleeding. Clinicians may use a head torch to identify any bleeding points, which may be actively bleeding or appear as fresh red clots. It is important to note that the tonsillar fossa may appear white or yellow, which is a normal postoperative finding.

Investigations such as a full blood count, coagulation profile, group and save, and venous blood gas may be performed to assess the patient’s condition. Senior support from ENT or anesthesiology should be called if there is active bleeding.

Management of post-tonsillectomy bleeding includes positioning the patient upright and keeping them calm, establishing intravenous access, administering fluids and blood products as needed, and administering tranexamic acid to stop bleeding. Bleeding points may require gentle suction removal of fresh clots, and topical medications such as Co-phenylcaine spray or topical adrenaline may be applied to the oropharynx. All patients with post-tonsillectomy bleeding should be assessed by ENT and observed for a prolonged period, typically 12-24 hours.

If bleeding remains uncontrolled, the patient should be kept nil by mouth in preparation for surgery, and early intervention.

NSAIDs are known to have a relaxing effect on the ureter, but a randomized controlled trial found no difference between NSAIDs and a placebo in terms of this effect. Currently, only two classes of drugs, calcium channel blockers and alpha-blockers, are considered effective as medical expulsive therapy (MET). Calcium channel blockers work by blocking the active calcium channel pump that the smooth muscle of the ureter uses to contract, resulting in relaxation of the muscle and improved stone passage. Alpha-blockers, on the other hand, are commonly used as the first-line treatment to enhance stone passage. They reduce the basal tone of the ureter smooth muscle, decrease the frequency of peristaltic waves, and lower ureteric contraction. This leads to a decrease in intraureteric pressure below the stone, increasing the chances of stone passage. Patients treated with calcium channel blockers or alpha-blockers have been shown to have a 65% higher likelihood of spontaneous stone passage compared to those not given these medications.

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 has been an improvement in safety procedures and a reduction in transfusion use, errors and serious adverse reactions still occur and often go unreported.

Mild allergic reactions during blood transfusion are relatively common and typically occur within a few minutes of starting the transfusion. These reactions happen when patients have antibodies that react with foreign plasma proteins in the transfused blood components. Symptoms of mild allergic reactions include urticaria, Pruritus, and hives.

Anaphylaxis, on the other hand, is much rarer and occurs when an individual has previously been sensitized to an allergen present in the blood. When re-exposed to the allergen, the body releases IgE or IgG antibodies, leading to severe symptoms such as bronchospasm, laryngospasm, abdominal pain, nausea, vomiting, hypotension, shock, and loss of consciousness. Anaphylaxis can be fatal.

Mild allergic reactions can be managed by slowing down the transfusion rate and administering antihistamines. If there is no progression after 30 minutes, the transfusion may continue. Patients who have experienced repeated allergic reactions to transfusion should be given pre-treatment with chlorpheniramine. In cases of anaphylaxis, the transfusion should be stopped immediately, and the patient should receive oxygen, adrenaline, corticosteroids, and antihistamines following the ALS protocol.

The table below summarizes the main transfusion reactions and complications, along with their features and management:

Complication | Features | Management
Febrile transfusion reaction | 1 degree rise in temperature, chills, malaise | Supportive care, paracetamol
Acute haemolytic reaction | Fever, chills, pain at transfusion site, nausea, vomiting, dark urine | STOP THE TRANSFUSION, administer IV fluids, diuretics if necessary
Delayed haemolytic reaction | Fever, anaemia, jaundice, haemoglobinuria | Monitor anaemia and renal function, treat as required
Allergic reaction | Urticaria, Pruritus, hives | Symptomatic treatment with ant

Tension pneumothorax is a condition characterized by certain clinical signs. These signs include pulsus paradoxus, which is an abnormal decrease in blood pressure during inspiration; elevated JVP or distended neck veins; diaphoresis or excessive sweating; and cyanosis, which is a bluish discoloration of the skin. Tracheal deviation to the left is often observed in patients with a right-sided pneumothorax. On the affected side, hyper-resonance and absent breath sounds can be expected. Patients with tension pneumothorax typically appear agitated and distressed, and they experience noticeable difficulty in breathing. Hypotension, a pulse rate exceeding 135 bpm, pulsus paradoxus, and elevated JVP are additional signs associated with tension pneumothorax. These signs occur because the expanding pneumothorax compresses the mediastinum, leading to impaired venous return and cardiac output.

Further Reading:

A pneumothorax is an abnormal collection of air in the pleural cavity of the lung. It can be classified by cause as primary spontaneous, secondary spontaneous, or traumatic. Primary spontaneous pneumothorax occurs without any obvious cause in the absence of underlying lung disease, while secondary spontaneous pneumothorax occurs in patients with significant underlying lung diseases. Traumatic pneumothorax is caused by trauma to the lung, often from blunt or penetrating chest wall injuries.

Tension pneumothorax is a life-threatening condition where the collection of air in the pleural cavity expands and compresses normal lung tissue and mediastinal structures. It can be caused by any of the aforementioned types of pneumothorax. Immediate management of tension pneumothorax involves the ABCDE approach, which includes ensuring a patent airway, controlling the C-spine, providing supplemental oxygen, establishing IV access for fluid resuscitation, and assessing and managing other injuries.

Treatment of tension pneumothorax involves needle thoracocentesis as a temporary measure to provide immediate decompression, followed by tube thoracostomy as definitive management. Needle thoracocentesis involves inserting a 14g cannula into the pleural space, typically via the 4th or 5th intercostal space midaxillary line. If the patient is peri-arrest, immediate thoracostomy is advised.

The pathophysiology of tension pneumothorax involves disruption to the visceral or parietal pleura, allowing air to flow into the pleural space. This can occur through an injury to the lung parenchyma and visceral pleura, or through an entry wound to the external chest wall in the case of a sucking pneumothorax. Injured tissue forms a one-way valve, allowing air to enter the pleural space with inhalation but prohibiting air outflow. This leads to a progressive increase in the volume of non-absorbable intrapleural air with each inspiration, causing pleural volume and pressure to rise within the affected hemithorax.

An overdose of Amitriptyline can lead to the development of an anticholinergic toxidrome. This toxidrome is characterized by various symptoms, which can be remembered using the phrase ‘mad as a hatter, hot as hell, red as a beat, dry as a bone, and blind as a bat’. Some of these symptoms include a dry mouth and an elevated body temperature.

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.

The FeverPAIN score is a scoring system recommended by the current NICE guidelines for assessing acute sore throats. It consists of five items: fever in the last 24 hours, purulence, attendance within three days, inflamed tonsils, and no cough or coryza. Based on the score, recommendations for antibiotic use are as follows: a score of 0-1 indicates an unlikely streptococcal infection, with antibiotics not recommended; a score of 2-3 suggests a 34-40% chance of streptococcus, and delayed prescribing of antibiotics may be considered; a score of 4 or higher indicates a 62-65% chance of streptococcus, and immediate antibiotic use is recommended for severe cases, or a short back-up prescription may be given for 48 hours.

The Fever PAIN score was developed through a study involving 1760 adults and children aged three and over. It was tested in a trial comparing three prescribing strategies: empirical delayed prescribing, score-directed prescribing, and a combination of the score with a near-patient test (NPT) for streptococcus. The use of the score resulted in faster symptom resolution and reduced antibiotic prescribing by one third. The addition of the NPT did not provide any additional benefit.

According to the current NICE guidelines, if antibiotics are necessary, phenoxymethylpenicillin is recommended as the first-choice antibiotic. In cases of true penicillin allergy, clarithromycin can be used as an alternative. For pregnant women with a penicillin allergy, erythromycin is prescribed. It is important to note that the threshold for prescribing antibiotics should be lower for individuals at risk of rheumatic fever and vulnerable groups managed in primary care, such as infants, the elderly, and those who are immunosuppressed or immunocompromised. Antibiotics should not be withheld if the person has severe symptoms and there are concerns about their clinical condition.

This patient has experienced otic barotrauma, which is most commonly seen during aircraft descent but can also occur in divers. Otic barotrauma occurs when the eustachian tube fails to equalize the pressure between the middle ear and the atmosphere, resulting in a pressure difference. This is more likely to happen in patients with eustachian tube dysfunction, such as those with acute otitis media or glue ear.

Patients with otic barotrauma often complain of severe ear pain, conductive hearing loss, ringing in the ears (tinnitus), and dizziness (vertigo). Upon examination, fluid can be observed behind the eardrum, and in more severe cases, the eardrum may even rupture.

In most instances, the symptoms of otic barotrauma resolve within a few days without any treatment. However, in more severe cases, it may take 2-3 weeks for the symptoms to subside. Nasal decongestants can be beneficial before and during a flight, but their effectiveness is limited once symptoms have already developed. Nasal steroids have no role in the management of otic barotrauma, and antibiotics should only be used if an infection develops.

The most appropriate course of action in this case would be to provide the patient with an explanation of what has occurred and reassure them that their symptoms should improve soon.