This patient is likely experiencing an acute coronary syndrome, possibly a non-ST-elevation myocardial infarction (NSTEMI) or unstable angina. The troponin test will help confirm the diagnosis. The patient’s ECG showed ST depression in the inferior leads, but this normalized after treatment with GTN and morphine, ruling out a ST-elevation myocardial infarction (STEMI).

Immediate pain relief should be provided. GTN (sublingual or buccal) can be used, but intravenous opioids like morphine should be considered, especially if a heart attack is suspected.

Aspirin should be given to all patients with unstable angina or NSTEMI as soon as possible and continued indefinitely, unless there are contraindications like bleeding risk or aspirin hypersensitivity. A loading dose of 300 mg should be administered right after presentation.

Fondaparinux should be given to patients without a high bleeding risk, unless coronary angiography is planned within 24 hours of admission. Unfractionated heparin can be an alternative to fondaparinux for patients who will undergo coronary angiography within 24 hours. For patients with significant renal impairment, unfractionated heparin can also be considered, with dose adjustment based on clotting function monitoring.

Routine administration of oxygen is no longer recommended, but oxygen saturation should be monitored using pulse oximetry as soon as possible, preferably before hospital admission. Supplemental oxygen should only be offered to individuals with oxygen saturation (SpO2) below 94% who are not at risk of hypercapnic respiratory failure, aiming for a SpO2 of 94-98%. For individuals with chronic obstructive pulmonary disease at risk of hypercapnic respiratory failure, a target SpO2 of 88-92% should be achieved until blood gas analysis is available.

Bivalirudin, a specific and reversible direct thrombin inhibitor (DTI), is recommended by NICE as a possible treatment for adults with STEMI undergoing percutaneous coronary intervention.

For more information, refer to the NICE guidelines on the assessment and diagnosis of chest pain of recent onset.

Multiple sclerosis is a condition characterized by the demyelination of nerve cells in the brain and spinal cord. It is an autoimmune disease mediated by cells and is caused by recurring inflammation. Typically, it presents in early adulthood, with a female to male ratio of 3:2.

There are several risk factors associated with multiple sclerosis, including being of Caucasian race, living at a greater distance from the equator (as the risk tends to be higher), having a family history of the disease (with 20% of MS patients having an affected relative), and smoking. Interestingly, the rates of relapse tend to decrease during pregnancy.

There are three main patterns of multiple sclerosis. The most common is relapsing and remitting MS, which is characterized by periods of no symptoms followed by relapses (this is seen in 80% of patients at the time of diagnosis). Another pattern is primary progressive MS, where symptoms develop and worsen from the beginning with few remissions (seen in 10-15% of patients at diagnosis). Lastly, there is secondary progressive MS, which occurs after relapsing/remitting MS. In this pattern, symptoms worsen with fewer remissions, and approximately 50% of those with relapsing/remitting MS will develop this within 10 years of diagnosis.

The key to diagnosing MS lies in the history of neurological symptoms that are discrete in time and location of the affected body. Patients often experience fatigue and low mood, particularly during a relapse.

Bier’s block is a regional intravenous anesthesia technique commonly used for minor surgical procedures of the forearm or for reducing distal radius fractures in the emergency department (ED). It is recommended by NICE as the preferred anesthesia block for adults requiring manipulation of distal forearm fractures in the ED.

Before performing the procedure, a pre-procedure checklist should be completed, including obtaining consent, recording the patient’s weight, ensuring the resuscitative equipment is available, and monitoring the patient’s vital signs throughout the procedure. The air cylinder should be checked if not using an electronic machine, and the cuff should be checked for leaks.

During the procedure, a double cuff tourniquet is placed on the upper arm, and the arm is elevated to exsanguinate the limb. The proximal cuff is inflated to a pressure 100 mmHg above the systolic blood pressure, up to a maximum of 300 mmHg. The time of inflation and pressure should be recorded, and the absence of the radial pulse should be confirmed. 0.5% plain prilocaine is then injected slowly, and the time of injection is recorded. The patient should be warned about the potential cold/hot sensation and mottled appearance of the arm. After injection, the cannula is removed and pressure is applied to the venipuncture site to prevent bleeding. After approximately 10 minutes, the patient should have anesthesia and should not feel pain during manipulation. If anesthesia is successful, the manipulation can be performed, and a plaster can be applied by a second staff member. A check x-ray should be obtained with the arm lowered onto a pillow. The tourniquet should be monitored at all times, and the cuff should be inflated for a minimum of 20 minutes and a maximum of 45 minutes. If rotation of the cuff is required, it should be done after the manipulation and plaster application. After the post-reduction x-ray is satisfactory, the cuff can be deflated while observing the patient and monitors. Limb circulation should be checked prior to discharge, and appropriate follow-up and analgesia should be arranged.

There are several contraindications to performing Bier’s block, including allergy to local anesthetic, hypertension over 200 mm Hg, infection in the limb, lymphedema, methemoglobinemia, morbid obesity, peripheral vascular disease, procedures needed in both arms, Raynaud’s phenomenon, scleroderma, severe hypertension and sickle cell disease.

Heat stroke is a condition characterized by a core temperature greater than 40.6°C, accompanied by changes in mental state and varying levels of organ dysfunction. There are two forms of heat stroke: classic non-exertional heat stroke, which occurs during high environmental temperatures and typically affects elderly patients during heat waves, and exertional heat stroke, which occurs during strenuous physical exercise in high environmental temperatures, such as endurance athletes competing in hot conditions. Heat stroke happens when the body’s thermoregulation is overwhelmed by excessive environmental heat, excessive metabolic heat production, and insufficient heat loss.

Several risk factors increase the likelihood of developing heat stroke. These include hot and humid environmental conditions, age (with the elderly and infants being particularly vulnerable), physical factors like obesity, excessive exertion, and dehydration, as well as medical comorbidities such as anorexia, cardiovascular disease, skin conditions, poorly controlled diabetes, Parkinson’s disease, and thyrotoxicosis. Certain drugs, including alcohol, amphetamines, anticholinergics, beta-blockers, cocaine, diuretics, phenothiazines, SSRIs, and sympathomimetics, can also increase the risk of heat stroke.

The typical clinical features of heat stroke include a core temperature greater than 40.6°C. Early signs may include extreme fatigue, headache, syncope, facial flushing, vomiting, and diarrhea. The skin is usually hot and dry, although sweating can occur in around 50% of cases of exertional heat stroke. The loss of the ability to sweat is a late and concerning sign. Hyperventilation is almost always present. Heat stroke can also lead to cardiovascular dysfunction, such as arrhythmias, hypotension, and shock, respiratory dysfunction including acute respiratory distress syndrome (ARDS), and central nervous system dysfunction, including seizures and coma. If the temperature rises above 41.5°C, multi-organ failure, coagulopathy, and rhabdomyolysis can occur.

Heat cramps, on the other hand, typically present with intense thirst and muscle cramps. Body temperature is often elevated but usually remains below 40°C. Sweating, heat dissipation mechanisms, and cognition are preserved, and there is no neurological impairment.

Heat exhaustion usually precedes heat stroke and, if left untreated, can progress to heat stroke. Heat dissipation is still functioning, and the body temperature is usually below 41°C.

Typhoid fever is a bacterial infection caused by Salmonella typhi. Paratyphoid fever, on the other hand, is a similar illness caused by Salmonella paratyphi. Together, these two conditions are collectively known as the enteric fevers.

Typhoid fever is prevalent in India and many other parts of Asia, Africa, Central America, and South America. It is primarily transmitted through the consumption of contaminated food or water that has been infected by the feces of an acutely infected or recovering person, or a chronic carrier. About 1-6% of individuals infected with S. typhi become chronic carriers. The incubation period for this illness ranges from 7 to 21 days.

During the first week of the illness, patients experience weakness and lethargy, accompanied by a gradually increasing fever. The onset of the illness is usually subtle, and constipation is more common than diarrhea in the early stages. Other early symptoms include headaches, abdominal pain, and nosebleeds. In cases of typhoid fever, the fever can occur with a relatively slow heart rate, known as Faget’s sign.

As the illness progresses into the second week, patients often become too fatigued to get out of bed. Diarrhea becomes more prominent, the fever intensifies, and patients may become agitated and delirious. The abdomen may become tender and swollen, and approximately 75% of patients develop an enlarged spleen. In up to a third of patients, red macules known as Rose spots may appear.

In the third week, the illness can lead to various complications. Intestinal bleeding may occur due to bleeding in congested Peyer’s patches. Other potential complications include intestinal perforation, secondary pneumonia, encephalitis, myocarditis, metastatic abscesses, and septic shock.

After the third week, surviving patients begin to show signs of improvement, with the fever and symptoms gradually subsiding over the course of 7-14 days. Untreated patients have a mortality rate of 15-30%. Traditionally, drugs like ampicillin and trimethoprim have been used for treatment. However, due to the emergence of multidrug resistant cases, azithromycin or fluoroquinolones are now the primary treatment options.

Carboxyhaemoglobin (COHb) blood levels are utilized for the identification of carbon monoxide poisoning. COHb is the substance produced when carbon monoxide attaches to haemoglobin. It is important to note that carbaminohemoglobin (also known as carbaminohaemoglobin, carboxyhemoglobin, and carbohemoglobin) is the compound formed when carbon dioxide binds to hemoglobin, and should not be mistaken for COHb.

Further Reading:

Carbon monoxide (CO) is a dangerous gas that is produced by the combustion of hydrocarbon fuels and can be found in certain chemicals. It is colorless and odorless, making it difficult to detect. In England and Wales, there are approximately 60 deaths each year due to accidental CO poisoning.

When inhaled, carbon monoxide binds to haemoglobin in the blood, forming carboxyhaemoglobin (COHb). It has a higher affinity for haemoglobin than oxygen, causing a left-shift in the oxygen dissociation curve and resulting in tissue hypoxia. This means that even though there may be a normal level of oxygen in the blood, it is less readily released to the tissues.

The clinical features of carbon monoxide toxicity can vary depending on the severity of the poisoning. Mild or chronic poisoning may present with symptoms such as headache, nausea, vomiting, vertigo, confusion, and weakness. More severe poisoning can lead to intoxication, personality changes, breathlessness, pink skin and mucosae, hyperpyrexia, arrhythmias, seizures, blurred vision or blindness, deafness, extrapyramidal features, coma, or even death.

To help diagnose domestic carbon monoxide poisoning, there are four key questions that can be asked using the COMA acronym. These questions include asking about co-habitees and co-occupants in the house, whether symptoms improve outside of the house, the maintenance of boilers and cooking appliances, and the presence of a functioning CO alarm.

Typical carboxyhaemoglobin levels can vary depending on whether the individual is a smoker or non-smoker. Non-smokers typically have levels below 3%, while smokers may have levels below 10%. Symptomatic individuals usually have levels between 10-30%, and severe toxicity is indicated by levels above 30%.

When managing carbon monoxide poisoning, the first step is to administer 100% oxygen. Hyperbaric oxygen therapy may be considered for individuals with a COHb concentration of over 20% and additional risk factors such as loss of consciousness, neurological signs, myocardial ischemia or arrhythmia, or pregnancy. Other management strategies may include fluid resuscitation, sodium bicarbonate for metabolic acidosis, and mannitol for cerebral edema.

The Lake Louise score is widely accepted as the standard method for evaluating the seriousness of Acute Mountain Sickness (AMS). The scoring system, outlined below, is used to determine the severity of AMS. A score of 3 or higher is indicative of AMS.

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.

Urinary tract stones form when the concentration of salt and minerals in the urine becomes too high. These stones can be classified into five types based on their mineral composition and how they develop.

The most common type of stone is the calcium stone, which can be further divided into calcium oxalate and calcium phosphate stones. These account for 60-80% of all urinary tract stones.

Another type is the struvite or magnesium ammonium phosphate stone, making up about 10-15% of cases. Uric acid stones, also known as urate stones, occur in 3-10% of cases.

Cystine stones are less common, accounting for less than 2% of urinary tract stones. Finally, there are drug-induced stones, which are caused by certain medications such as triamterene, protease inhibitors like indinavir sulphate, and sulfa drugs. These account for approximately 1% of cases.

By understanding the different types of urinary tract stones, healthcare professionals can better diagnose and treat patients with this condition.

Early assessment of the airway is a critical aspect of managing a patient who has suffered burns. Airway blockage can occur rapidly due to direct injury, such as inhalation injury, or as a result of swelling caused by the burn. If there is a history of trauma, the airway should be evaluated and treated while maintaining control of the cervical spine.

Signs of airway obstruction may not be immediately apparent, as swelling typically does not occur right away. Children with thermal burns are at a higher risk of airway obstruction compared to adults due to their smaller airway size, so they require careful observation.

There are several risk factors for airway obstruction in burned patients, including inhalation injury, the presence of soot in the mouth or nostrils, singed nasal hairs, burns to the head, face, or neck, burns inside the mouth, a large burn area with increasing depth, and associated trauma. A carboxyhemoglobin level above 10% is also suggestive of an inhalation injury.

Thiopental sodium is a barbiturate with a very short duration of action. It is primarily used to induce anesthesia. Barbiturates are believed to primarily affect synapses by reducing the sensitivity of postsynaptic receptors to neurotransmitters and by interfering with the release of neurotransmitters from presynaptic neurons.

Thiopental sodium specifically binds to a unique site associated with a chloride ionophore at the GABAA receptor, which is responsible for the opening of chloride ion channels. This binding increases the length of time that the chloride ionophore remains open. As a result, the inhibitory effect of GABA on postsynaptic neurons in the thalamus is prolonged.

In summary, thiopental sodium acts as a short-acting barbiturate that is commonly used to induce anesthesia. It affects synapses by reducing postsynaptic receptor sensitivity and interfering with neurotransmitter release. By binding to a specific site at the GABAA receptor, thiopental sodium prolongs the inhibitory effect of GABA in the thalamus.

The earliest and most frequent clinical indication of malignant hyperthermia is typically an increase in end tidal CO2. An unexplained elevation in end tidal CO2 is often the initial and most reliable sign of this condition.

Further Reading:

Malignant hyperthermia is a rare and life-threatening syndrome that can be triggered by certain medications in individuals who are genetically susceptible. The most common triggers are suxamethonium and inhalational anaesthetic agents. The syndrome is caused by the release of stored calcium ions from skeletal muscle cells, leading to uncontrolled muscle contraction and excessive heat production. This results in symptoms such as high fever, sweating, flushed skin, rapid heartbeat, and muscle rigidity. It can also lead to complications such as acute kidney injury, rhabdomyolysis, and metabolic acidosis. Treatment involves discontinuing the trigger medication, administering dantrolene to inhibit calcium release and promote muscle relaxation, and managing any associated complications such as hyperkalemia and acidosis. Referral to a malignant hyperthermia center for further investigation is also recommended.

An acoustic neuroma, also referred to as a vestibular schwannoma, is a slow-growing tumor that develops from the Schwann cells of the vestibulocochlear nerve (8th cranial nerve). These growths are typically found at the cerebellopontine angle or within the internal auditory canal.

The most commonly affected nerves are the vestibulocochlear and trigeminal nerves. Patients typically experience a gradual deterioration of hearing in one ear, along with numbness and tingling in the face, ringing in the ears, and episodes of dizziness. Headaches may also be present, and in rare cases, the facial nerve, glossopharyngeal nerve, vagus nerve, or accessory nerve may be affected.

It’s important to note that the trochlear nerve, which passes through the superior orbital fissure, is not impacted by an acoustic neuroma.

Traumatic aortic rupture, also known as traumatic aortic disruption or transection, occurs when the aorta is torn or ruptured due to physical trauma. This condition often leads to sudden death because of severe bleeding. Motor vehicle accidents and falls from great heights are the most common causes of this injury.

The patients with the highest chances of survival are those who have an incomplete tear near the ligamentum arteriosum of the proximal descending aorta, close to where the left subclavian artery branches off. The presence of an intact adventitial layer or contained mediastinal hematoma helps maintain continuity and prevents immediate bleeding and death. If promptly identified and treated, survivors of these injuries can recover. In cases where traumatic aortic rupture leads to sudden death, approximately 50% of patients have damage at the aortic isthmus, while around 15% have damage in either the ascending aorta or the aortic arch.

Initial chest X-rays may show signs consistent with a traumatic aortic injury. However, false-positive and false-negative results can occur, and sometimes there may be no abnormalities visible on the X-ray. Some of the possible X-ray findings include a widened mediastinum, hazy left lung field, obliteration of the aortic knob, fractures of the 1st and 2nd ribs, deviation of the trachea to the right, presence of a pleural cap, elevation and rightward shift of the right mainstem bronchus, depression of the left mainstem bronchus, obliteration of the space between the pulmonary artery and aorta, and deviation of the esophagus or NG tube to the right.

A helical contrast-enhanced CT scan of the chest is the preferred initial investigation for suspected blunt aortic injury. It has proven to be highly accurate, with close to 100% sensitivity and specificity. CT scanning should be performed liberally, as chest X-ray findings can be unreliable. However, hemodynamically unstable patients should not be placed in a CT scanner. If the CT results are inconclusive, aortography or trans-oesophageal echo can be performed for further evaluation.

Immediate surgical intervention is necessary for these injuries. Endovascular repair is the most common method used and has excellent short-term outcomes. Open repair may also be performed depending on the circumstances. It is important to control heart rate and blood pressure during stabilization to reduce the risk of rupture. Pain should be managed with appropriate analgesic

Potassium-sparing diuretics, like spironolactone and eplerenone, can raise the chances of developing hyperkalemia when taken alongside ACE inhibitors, such as ramipril, and angiotensin-II receptor antagonists, like losartan. Additionally, eplerenone can also heighten the risk of hypotension when co-administered with losartan.

For more information, please refer to the BNF section on losartan interactions.

Methanol poisoning is linked to an increase in anion gap acidosis.

Further Reading:

Arterial blood gases (ABG) are an important diagnostic tool used to assess a patient’s acid-base status and respiratory function. When obtaining an ABG sample, it is crucial to prioritize safety measures to minimize the risk of infection and harm to the patient. This includes performing hand hygiene before and after the procedure, wearing gloves and protective equipment, disinfecting the puncture site with alcohol, using safety needles when available, and properly disposing of equipment in sharps bins and contaminated waste bins.

To reduce the risk of harm to the patient, it is important to test for collateral circulation using the modified Allen test for radial artery puncture. Additionally, it is essential to inquire about any occlusive vascular conditions or anticoagulation therapy that may affect the procedure. The puncture site should be checked for signs of infection, injury, or previous surgery. After the test, pressure should be applied to the puncture site or the patient should be advised to apply pressure for at least 5 minutes to prevent bleeding.

Interpreting ABG results requires a systematic approach. The core set of results obtained from a blood gas analyser includes the partial pressures of oxygen and carbon dioxide, pH, bicarbonate concentration, and base excess. These values are used to assess the patient’s acid-base status.

The pH value indicates whether the patient is in acidosis, alkalosis, or within the normal range. A pH less than 7.35 indicates acidosis, while a pH greater than 7.45 indicates alkalosis.

The respiratory system is assessed by looking at the partial pressure of carbon dioxide (pCO2). An elevated pCO2 contributes to acidosis, while a low pCO2 contributes to alkalosis.

The metabolic aspect is assessed by looking at the bicarbonate (HCO3-) level and the base excess. A high bicarbonate concentration and base excess indicate alkalosis, while a low bicarbonate concentration and base excess indicate acidosis.

Analyzing the pCO2 and base excess values can help determine the primary disturbance and whether compensation is occurring. For example, a respiratory acidosis (elevated pCO2) may be accompanied by metabolic alkalosis (elevated base excess) as a compensatory response.

The anion gap is another important parameter that can help determine the cause of acidosis. It is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium.

The main sensory supply to the back of the scalp comes from the C2 and C3 cervical nerves. The scalp receives innervation from branches of both the trigeminal nerve and the cervical nerves, as depicted in the illustration in the notes. The C2 and C3 cervical nerves are primarily responsible for supplying sensation to the posterior scalp.

Further Reading:

The scalp is the area of the head that is bordered by the face in the front and the neck on the sides and back. It consists of several layers, including the skin, connective tissue, aponeurosis, loose connective tissue, and periosteum of the skull. These layers provide protection and support to the underlying structures of the head.

The blood supply to the scalp primarily comes from branches of the external carotid artery and the ophthalmic artery, which is a branch of the internal carotid artery. These arteries provide oxygen and nutrients to the scalp tissues.

The scalp also has a complex venous drainage system, which is divided into superficial and deep networks. The superficial veins correspond to the arterial branches and are responsible for draining blood from the scalp. The deep venous network is drained by the pterygoid venous plexus.

In terms of innervation, the scalp receives sensory input from branches of the trigeminal nerve and the cervical nerves. These nerves transmit sensory information from the scalp to the brain, allowing us to perceive touch, pain, and temperature in this area.

Cauda equina syndrome (CES) is a rare but serious complication that can occur when a disc ruptures. This happens when the material from the disc is pushed into the spinal canal and puts pressure on the bundle of nerves in the lower back and sacrum. As a result, individuals may experience loss of control over their bladder and bowel functions.

There are certain red flags that may indicate the presence of CES. These include experiencing sciatica on both sides of the body, having severe or worsening neurological issues in both legs (such as significant weakness in knee extension, ankle eversion, or foot dorsiflexion), difficulty starting urination or a decreased sensation of urinary flow, loss of sensation in the rectum, experiencing numbness or tingling in the perianal, perineal, or genital areas (also known as saddle anesthesia or paresthesia), and having a lax anal sphincter.

Conus medullaris syndrome (CMS) is a condition that affects the conus medullaris, which is located above the cauda equina at the T12-L2 level. Unlike CES, CMS primarily causes back pain and may have less noticeable nerve root pain. The main symptoms of CMS are urinary retention and constipation.

To confirm a diagnosis of CES and determine the level of compression and any underlying causes, an MRI scan is considered the gold-standard investigation. In cases where an MRI is not possible or contraindicated, a CT myelogram or standard CT scans can be helpful. However, plain radiographs have limited value and may only show significant degenerative or traumatic bone diseases.

Von Willebrand disease (vWD) is a common hereditary coagulation disorder that affects about 1 in 100 people. It occurs due to a deficiency in Von Willebrand factor (vWF), which is responsible for protecting factor VIII from breaking down too quickly in the blood. Additionally, vWF is necessary for proper platelet adhesion, so a lack of it can lead to abnormal platelet function. As a result, both the APTT and bleeding time are prolonged, while the platelet count and thrombin time remain unaffected.

In many cases, vWD goes unnoticed as patients do not experience any symptoms. It is often diagnosed incidentally during a routine clotting profile check. However, if symptoms do occur, the most common ones are easy bruising, nosebleeds, and heavy menstrual bleeding. In severe cases, more serious bleeding and joint bleeds can occur.

For mild cases of von Willebrand disease, bleeding can be treated with desmopressin. This medication helps increase the patient’s own levels of vWF by releasing stored vWF from the Weibel-Palade bodies in the endothelial cells. These bodies are storage granules found in the inner lining of blood vessels and the heart. In more severe cases, replacement therapy is necessary, which involves infusing cryoprecipitate or Factor VIII concentrate. Replacement therapy is recommended for patients with severe von Willebrand’s disease who are undergoing moderate or major surgical procedures.

In an elderly patient with a history of gradual decline accompanied by symptoms of hyperglycemia, excessive thirst, recent infection, and very high blood sugar levels, the most likely diagnosis is a hyperosmolar hyperglycemic state (HHS). This condition can be life-threatening, with a mortality rate of approximately 50%. Common symptoms include high blood sugar levels, dehydration, altered mental status, and electrolyte imbalances. About 50% of patients with HHS also experience hypernatremia, an elevated sodium level in the blood.

To calculate the serum osmolality, the following formula can be used: 2 (K+ + Na+) + urea + glucose. In this particular case, the calculation would be 2 (3.2 + 154) + 17.6 + 32 = 364 mmol/l. Patients with HHS typically have a serum osmolality greater than 350 mmol/l.

In order to manage HHS, it is important to address the underlying cause and gradually and safely achieve the following goals:
1. Normalize the osmolality
2. Replace fluid and electrolyte losses
3. Normalize blood glucose levels

Given the presence of 1+ ketones in the patient’s urine, which is likely due to vomiting and a mild acidosis, it is recommended to discontinue the use of metformin due to the risk of metformin-associated lactic acidosis (MALA). Additionally, an intravenous infusion of insulin should be initiated in this case.

If significant ketonaemia is present (3β-hydroxybutyrate is more than 1 mmol/L), it indicates a relative deficiency of insulin, and insulin treatment should be started immediately. However, if significant ketonaemia is not present, insulin should not be initiated.

Patients with HHS are at a high risk of developing thromboembolism, and therefore, routine administration of low molecular weight heparin is recommended. In cases where the serum osmolality exceeds 350 mmol/l, full heparinization should be considered.

The current guidelines from NICE provide recommendations for managing low back pain. It is suggested to consider using oral non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, while taking into account the potential risks of gastrointestinal, liver, and cardio-renal toxicity, as well as the person’s individual risk factors and age. When prescribing oral NSAIDs, it is important to conduct appropriate clinical assessments, monitor risk factors regularly, and consider the use of gastroprotective treatment. It is advised to prescribe the lowest effective dose of oral NSAIDs for the shortest duration possible. In cases where NSAIDs are contraindicated, not tolerated, or ineffective, weak opioids (with or without paracetamol) may be considered for managing acute low back pain. However, NICE does not recommend the use of paracetamol alone, opioids for chronic low back pain, serotonin reuptake inhibitors, serotonin-noradrenaline reuptake inhibitors, tricyclic antidepressants for non-neuropathic pain, anticonvulsants, or benzodiazepines for muscle spasm associated with acute low back pain. For more information, you can refer to the NICE guidance on low back pain and sciatica in individuals over 16 years old, as well as the NICE Clinical Knowledge Summary on low back pain without radiculopathy.