Delirium is characterized by fluctuating symptoms of disturbed consciousness that typically develop over hours to days. During the day, lucid intervals may occur, while the worst disturbances are often experienced at night. In contrast, dementia has a gradual onset and does not involve fluctuations in mental state. Stroke, on the other hand, is associated with focal neurological deficits.

Further Reading:

Delirium is an acute syndrome that causes disturbances in consciousness, attention, cognition, and perception. It is also known as an acute confusional state. The DSM-IV criteria for diagnosing delirium include recent onset of fluctuating awareness, impairment of memory and attention, and disorganized thinking. Delirium typically develops over hours to days and may be accompanied by behavioral changes, personality changes, and psychotic features. It often occurs in individuals with predisposing factors, such as advanced age or multiple comorbidities, when exposed to new precipitating factors, such as medications or infection. Symptoms of delirium fluctuate throughout the day, with lucid intervals occurring during the day and worse disturbances at night. Falling and loss of appetite are often warning signs of delirium.

Delirium can be classified into three subtypes based on the person’s symptoms. Hyperactive delirium is characterized by inappropriate behavior, hallucinations, and agitation. Restlessness and wandering are common in this subtype. Hypoactive delirium is characterized by lethargy, reduced concentration, and appetite. The person may appear quiet or withdrawn. Mixed delirium presents with signs and symptoms of both hyperactive and hypoactive subtypes.

The exact pathophysiology of delirium is not fully understood, but it is believed to involve multiple mechanisms, including cholinergic deficiency, dopaminergic excess, and inflammation. The cause of delirium is usually multifactorial, with predisposing factors and precipitating factors playing a role. Predisposing factors include older age, cognitive impairment, frailty, significant injuries, and iatrogenic events. Precipitating factors include infection, metabolic or electrolyte disturbances, cardiovascular disorders, respiratory disorders, neurological disorders, endocrine disorders, urological disorders, gastrointestinal disorders, severe uncontrolled pain, alcohol intoxication or withdrawal, medication use, and psychosocial factors.

Delirium is highly prevalent in hospital settings, affecting up to 50% of inpatients aged over 65 and occurring in 30% of people aged over 65 presenting to the emergency department. Complications of delirium include increased risk of death, high in-hospital mortality rates, higher mortality rates following hospital discharge, increased length of stay in hospital, nosocomial infections, increased risk of admission to long-term care or re-admission to hospital, increased incidence of dementia, increased risk of falls and associated injuries, pressure sores.

All patients who present with painless haematuria should undergo cystoscopy to rule out bladder cancer. This procedure is typically done in an outpatient setting as part of a haematuria clinic, using a flexible cystoscope and local anaesthetic.

In this case, the likelihood of prostate cancer is much lower due to the patient’s relatively normal prostate examination and mild symptoms of bladder outlet obstruction.

Bladder cancer is the seventh most common cancer in the UK, with men being three times more likely to develop it than women. The main risk factors for bladder cancer are increasing age and smoking. Approximately 50% of bladder cancers are caused by smoking, which is believed to be due to the presence of certain chemicals that are excreted through the kidneys. Smokers have a 2-6 times higher risk of developing bladder cancer compared to non-smokers.

Painless macroscopic haematuria is the most common symptom in 80-90% of bladder cancer cases. There are usually no abnormalities found during a standard physical examination.

According to current recommendations, the following patients should be urgently referred for a urological assessment:
– Adults over 45 years old with unexplained visible haematuria and no urinary tract infection.
– Adults over 45 years old with visible haematuria that persists or recurs after successful treatment of a urinary tract infection.
– Adults aged 60 and over with unexplained non-visible haematuria and either dysuria or an elevated white cell count on a blood test.

For those aged 60 and over with recurrent or persistent unexplained urinary tract infection, a non-urgent referral for bladder cancer is recommended.

The FeverPAIN score is a clinical scoring system that helps determine the likelihood of a streptococcal infection and whether antibiotic treatment is necessary. It consists of several criteria that are assessed to assign a score.

Firstly, if the patient has a fever higher than 38°C, they score 0 or 1 depending on the presence or absence of this symptom.

Secondly, the presence of purulence, such as pharyngeal or tonsillar exudate, results in a score of 1.

Thirdly, if the patient sought medical attention within 3 days or less, they score 1.

Fourthly, if the patient has severely inflamed tonsils, they score 1.

Lastly, if the patient does not have a cough or coryza (nasal congestion), they score 1.

By adding up the scores from each criterion, the FeverPAIN score can help healthcare professionals determine the likelihood of a streptococcal infection and guide the decision on whether antibiotic treatment is necessary. In this particular case, the patient has a score of 4.

Further Reading:

Pharyngitis and tonsillitis are common conditions that cause inflammation in the throat. Pharyngitis refers to inflammation of the oropharynx, which is located behind the soft palate, while tonsillitis refers to inflammation of the tonsils. These conditions can be caused by a variety of pathogens, including viruses and bacteria. The most common viral causes include rhinovirus, coronavirus, parainfluenza virus, influenza types A and B, adenovirus, herpes simplex virus type 1, and Epstein Barr virus. The most common bacterial cause is Streptococcus pyogenes, also known as Group A beta-hemolytic streptococcus (GABHS). Other bacterial causes include Group C and G beta-hemolytic streptococci and Fusobacterium necrophorum.

Group A beta-hemolytic streptococcus is the most concerning pathogen as it can lead to serious complications such as rheumatic fever and glomerulonephritis. These complications can occur due to an autoimmune reaction triggered by antigen/antibody complex formation or from cell damage caused by bacterial exotoxins.

When assessing a patient with a sore throat, the clinician should inquire about the duration and severity of the illness, as well as associated symptoms such as fever, malaise, headache, and joint pain. It is important to identify any red flags and determine if the patient is immunocompromised. Previous non-suppurative complications of Group A beta-hemolytic streptococcus infection should also be considered, as there is an increased risk of further complications with subsequent infections.

Red flags that may indicate a more serious condition include severe pain, neck stiffness, or difficulty swallowing. These symptoms may suggest epiglottitis or a retropharyngeal abscess, which require immediate attention.

To determine the likelihood of a streptococcal infection and the need for antibiotic treatment, two scoring systems can be used: CENTOR and FeverPAIN. The CENTOR criteria include tonsillar exudate, tender anterior cervical lymphadenopathy or lymphadenitis, history of fever, and absence of cough. The FeverPAIN criteria include fever, purulence, rapid onset of symptoms, severely inflamed tonsils, and absence of cough or coryza. Based on the scores from these criteria, the likelihood of a streptococcal infection can be estimated, and appropriate management can be undertaken. can

Hyperkalaemia, or high levels of potassium in the blood, can be caused by various factors that are not related to drug use. These include conditions such as renal failure, where the kidneys are unable to properly regulate potassium levels, and excess potassium supplementation. Other non-drug causes include Addison’s disease, a condition characterized by adrenal insufficiency, and congenital adrenal hyperplasia. Renal tubular acidosis, specifically type 4, can also lead to hyperkalaemia. Additionally, conditions like rhabdomyolysis, burns and trauma, and tumour lysis syndrome can contribute to elevated potassium levels. Acidosis, an imbalance in the body’s pH levels, is another non-drug cause of hyperkalaemia.

On the other hand, certain medications have been associated with hyperkalaemia. These include ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium. These drugs can interfere with the body’s potassium regulation mechanisms and lead to increased levels of potassium in the blood.

In contrast, there are also conditions that result in low levels of potassium, known as hypokalaemia. Bartter’s syndrome, a rare inherited defect in the ascending limb of the loop of Henle, is characterized by hypokalaemic alkalosis and normal to low blood pressure. Type 1 and 2 renal tubular acidosis are other conditions that cause hypokalaemia. On the other hand, type 4 renal tubular acidosis leads to hyperkalaemia. Gitelman’s syndrome, another rare inherited defect, affects the distal convoluted tubule of the kidney and causes a metabolic alkalosis with hypokalaemia and hypomagnesaemia.

Lastly, excessive consumption of liquorice can result in a condition called hypermineralocorticoidism, which can lead to hypokalaemia.

In a child with a non-blanching rash, it is important to consider the possibility of meningococcal septicaemia. This is especially true if the child appears unwell, has purpura (lesions larger than 2 mm in diameter), a capillary refill time of more than 3 seconds, or neck stiffness. In the UK, most cases of meningococcal septicaemia are caused by Neisseria meningitidis group B.

In this particular case, the child is clearly very sick and showing signs of septic shock. It is crucial to administer a single dose of benzylpenicillin without delay and arrange for immediate transfer to the nearest Emergency Department via ambulance.

The recommended doses of benzylpenicillin based on age are as follows:
– Infants under 1 year of age: 300 mg of IM or IV benzylpenicillin
– Children aged 1 to 9 years: 600 mg of IM or IV benzylpenicillin
– Children and adults aged 10 years or older: 1.2 g of IM or IV benzylpenicillin.

Atropine acts as an antagonist to the parasympathetic neurotransmitter acetylcholine at muscarinic receptors. This means that it blocks the effects of the vagus nerve on both the SA node and the AV node, resulting in increased sinus automaticity and improved AV node conduction.

The side effects of atropine are dependent on the dosage and may include dry mouth, nausea and vomiting, blurred vision, urinary retention, and tachyarrhythmias. Elderly patients may also experience acute confusion and hallucinations.

Atropine is recommended for use in cases of sinus, atrial, or nodal bradycardia or AV block when the patient’s hemodynamic condition is unstable due to the bradycardia. According to the ALS bradycardia algorithm, an initial dose of 500 mcg IV is suggested if any adverse features such as shock, syncope, myocardial ischemia, or heart failure are present. If this initial dose is unsuccessful, additional 500 mcg doses can be administered at 3-5 minute intervals, with a maximum dose of 3 mg. It is important to avoid doses exceeding 3 mg as they can paradoxically slow the heart rate.

Asystole during cardiac arrest is typically caused by primary myocardial pathology rather than excessive vagal tone. Therefore, there is no evidence supporting the routine use of atropine in the treatment of asystole or PEA. Consequently, atropine is no longer included in the non-shockable part of the ALS algorithm.

Aside from its use in cardiac conditions, atropine also has other applications. It can be used topically in the eyes as a cycloplegic and mydriatic, to reduce secretions during anesthesia, and in the treatment of organophosphate poisoning.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This leads to the accumulation of urea and other waste products in the body, as well as disturbances in fluid balance and electrolyte levels. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease.

AKI is categorized into three stages based on specific criteria. In stage 1, there is a rise in creatinine levels of 26 micromol/L or more within 48 hours, or a rise of 50-99% from baseline within 7 days (1.5-1.99 times the baseline). Additionally, a urine output of less than 0.5 mL/kg/hour for more than 6 hours is indicative of stage 1 AKI.

Stage 2 AKI is characterized by a creatinine rise of 100-199% from baseline within 7 days (2.0-2.99 times the baseline), or a urine output of less than 0.5 mL/kg/hour for more than 12 hours.

In stage 3 AKI, there is a creatinine rise of 200% or more from baseline within 7 days (3.0 or more times the baseline). Alternatively, a creatinine rise to 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours, or a rise of 50% or more within 7 days, is indicative of stage 3 AKI. Additionally, a urine output of less than 0.3 mL/kg/hour for 24 hours or anuria (no urine output) for 12 hours also falls under stage 3 AKI.

Chagas disease, also known as American Trypanosomiasis, is a tropical illness caused by the protozoan Trypanosoma cruzi. It is transmitted by Triatomine insects, commonly known as kissing bugs, which belong to the Reduviidae family. This zoonotic disease is prevalent in Central and South America, with an estimated 8 million people infected in the region. In Brazil alone, there are approximately 120,000 new cases reported each year.

The disease progresses through two stages: the acute stage and the chronic stage. During the acute stage, many patients may not experience any symptoms, and the infection can go unnoticed. However, some individuals may exhibit symptoms such as fever, malaise, muscle pain, loss of appetite, and occasionally vomiting and diarrhea. Clinical signs may include swollen lymph nodes and enlargement of the liver and spleen. At the site of the insect bite, an inflammatory response called a chagoma can occur. This is characterized by a swollen, violet-colored nodule that can last up to 8 weeks. Another distinctive sign of acute Chagas disease is Romaña’s sign, which is eyelid swelling caused by accidentally rubbing bug feces into the eyes.

Following the acute stage, an estimated 10-30% of individuals progress to the chronic stage of Chagas disease. There is typically a latent phase between the acute and chronic phases, which can last for as long as 20-30 years. The chronic phase is associated with various complications, including cardiovascular problems such as dilated cardiomyopathy, heart failure, and arrhythmias. Gastrointestinal issues like megacolon, megaesophagus, and secondary achalasia can also arise. Neurological complications, such as neuritis, sensory and motor deficits, and encephalopathy, may occur. Additionally, psychiatric symptoms, including dementia, can manifest in some cases.

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.

Croup, also known as laryngo-tracheo-bronchitis, is typically caused by the parainfluenza virus. Other viruses such as rhinovirus, influenza, and respiratory syncytial viruses can also be responsible. Before the onset of stridor, there is often a mild cold-like illness that lasts for 1-2 days. Symptoms usually reach their peak within 1-3 days, with the cough often being more troublesome at night. A milder cough may persist for another 7-10 days.

A distinctive feature of croup is a barking cough, but it does not indicate the severity of the condition. To reduce airway swelling, dexamethasone and prednisolone are commonly prescribed. If a child is experiencing vomiting, nebulized budesonide can be used as an alternative. However, it is important to note that steroids do not shorten the duration of the illness. In severe cases, nebulized adrenaline can be administered.

Hospitalization for croup is uncommon and typically reserved for children who are experiencing worsening respiratory distress or showing signs of drowsiness or agitation.

The patient is experiencing acidosis, as indicated by the low pH. The low bicarb and base excess levels suggest that the metabolic system is contributing to or causing the acidosis. Additionally, the low pCO2 indicates that the respiratory system is attempting to compensate by driving alkalosis. However, the metabolic system is the primary factor in this case, leading to a diagnosis of metabolic acidosis with incomplete respiratory compensation.

Further Reading:

Salicylate poisoning, particularly from aspirin overdose, is a common cause of poisoning in the UK. One important concept to understand is that salicylate overdose leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the overdose stimulates the respiratory center, leading to hyperventilation and respiratory alkalosis. However, as the effects of salicylate on lactic acid production, breakdown into acidic metabolites, and acute renal injury occur, it can result in high anion gap metabolic acidosis.

The clinical features of salicylate poisoning include hyperventilation, tinnitus, lethargy, sweating, pyrexia (fever), nausea/vomiting, hyperglycemia and hypoglycemia, seizures, and coma.

When investigating salicylate poisoning, it is important to measure salicylate levels in the blood. The sample should be taken at least 2 hours after ingestion for symptomatic patients or 4 hours for asymptomatic patients. The measurement should be repeated every 2-3 hours until the levels start to decrease. Other investigations include arterial blood gas analysis, electrolyte levels (U&Es), complete blood count (FBC), coagulation studies (raised INR/PTR), urinary pH, and blood glucose levels.

To manage salicylate poisoning, an ABC approach should be followed to ensure a patent airway and adequate ventilation. Activated charcoal can be administered if the patient presents within 1 hour of ingestion. Oral or intravenous fluids should be given to optimize intravascular volume. Hypokalemia and hypoglycemia should be corrected. Urinary alkalinization with intravenous sodium bicarbonate can enhance the elimination of aspirin in the urine. In severe cases, hemodialysis may be necessary.

Urinary alkalinization involves targeting a urinary pH of 7.5-8.5 and checking it hourly. It is important to monitor for hypokalemia as alkalinization can cause potassium to shift from plasma into cells. Potassium levels should be checked every 1-2 hours.

In cases where the salicylate concentration is high (above 500 mg/L in adults or 350 mg/L in children), sodium bicarbonate can be administered intravenously. Hemodialysis is the treatment of choice for severe poisoning and may be indicated in cases of high salicylate levels, resistant metabolic acidosis, acute kidney injury, pulmonary edema, seizures and coma.

A 512 Hz tuning fork is recommended for conducting both the Rinne’s and Weber’s tests. However, a lower-pitched 128 Hz tuning fork is commonly used to assess vibration sense during a peripheral nervous system examination. Although a 256 Hz tuning fork can be used for both tests, it is considered less reliable.

To perform the Weber’s test, the 512 Hz tuning fork should be set in motion and then placed on the center of the patient’s forehead. The patient should be asked if they perceive the sound in the middle of their forehead or if it is heard more on one side.

If the sound is heard more on one side, it may indicate either ipsilateral conductive hearing loss or contralateral sensorineural hearing loss.

Aortic stenosis leads to the presence of a murmur during the ejection phase of the cardiac cycle. This murmur is most audible at the right second intercostal space and can be heard extending into the right neck.

Mitral regurgitation, on the other hand, produces a high-pitched murmur that occurs throughout the entire systolic phase of the cardiac cycle. This murmur is best heard at the apex of the heart and can be heard radiating into the axilla.

Tricuspid regurgitation is characterized by a blowing murmur that occurs throughout the entire systolic phase of the cardiac cycle. This murmur is most clearly heard at the lower left sternal edge.

Ventricular septal defect results in a harsh murmur that occurs throughout the entire systolic phase of the cardiac cycle. This murmur is best heard at the third or fourth left intercostal space and can be heard radiating throughout the praecordium.

Aortopulmonary shunts are an extremely rare cause of a murmur that occurs throughout the entire systolic phase of the cardiac cycle.

When a person’s systolic blood pressure is less than 90 mmHg, it indicates low blood pressure. A pulse rate above 100 or below 60 beats per minute is considered abnormal. An anion gap above 16 is indicative of an imbalance in the body’s electrolytes.

Further Reading:

Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

Addison’s disease is characterized by several classical biochemical features. One of these features is an elevated level of ACTH, which is the body’s attempt to stimulate the adrenal glands. Additionally, individuals with Addison’s disease often experience hyponatremia, which is a decrease in the level of sodium in the blood. Another common feature is hyperkalemia, which refers to an excessive amount of potassium in the blood. Furthermore, individuals with Addison’s disease may also experience hypercalcemia, which is an elevated level of calcium in the blood. Hypoglycemia, which is low blood sugar, is another characteristic feature of this disease. Lastly, metabolic acidosis, which refers to an imbalance in the body’s acid-base levels, is also commonly observed in individuals with Addison’s disease.

The key initial management for tension pneumothorax is needle thoracocentesis. This procedure is crucial as it rapidly decompresses the tension and allows for more definitive management to be implemented. It is important to note that according to ATLS guidelines, needle thoracocentesis should no longer be performed at the second intercostal space midclavicular line. Studies have shown that the fourth or fifth intercostal space midaxillary line is more successful in reaching the thoracic cavity in adult patients. Therefore, ATLS now recommends this location for needle decompression in adult patients.

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.

The FeverPAIN score is a clinical scoring system that helps determine the probability of streptococcal infection and the necessity of antibiotic treatment. NICE recommends using either the CENTOR or FeverPAIN clinical scoring systems to assess the likelihood of streptococcal infection and the need for antibiotics. The RSI score is utilized to evaluate laryngopharyngeal reflux, while the CSMCPI is employed to predict clinical outcomes in patients with upper gastrointestinal bleeding. Lastly, the Mallampati score is used to assess the oropharyngeal space and predict the difficulty of endotracheal intubation.

Further Reading:

Pharyngitis and tonsillitis are common conditions that cause inflammation in the throat. Pharyngitis refers to inflammation of the oropharynx, which is located behind the soft palate, while tonsillitis refers to inflammation of the tonsils. These conditions can be caused by a variety of pathogens, including viruses and bacteria. The most common viral causes include rhinovirus, coronavirus, parainfluenza virus, influenza types A and B, adenovirus, herpes simplex virus type 1, and Epstein Barr virus. The most common bacterial cause is Streptococcus pyogenes, also known as Group A beta-hemolytic streptococcus (GABHS). Other bacterial causes include Group C and G beta-hemolytic streptococci and Fusobacterium necrophorum.

Group A beta-hemolytic streptococcus is the most concerning pathogen as it can lead to serious complications such as rheumatic fever and glomerulonephritis. These complications can occur due to an autoimmune reaction triggered by antigen/antibody complex formation or from cell damage caused by bacterial exotoxins.

When assessing a patient with a sore throat, the clinician should inquire about the duration and severity of the illness, as well as associated symptoms such as fever, malaise, headache, and joint pain. It is important to identify any red flags and determine if the patient is immunocompromised. Previous non-suppurative complications of Group A beta-hemolytic streptococcus infection should also be considered, as there is an increased risk of further complications with subsequent infections.

Red flags that may indicate a more serious condition include severe pain, neck stiffness, or difficulty swallowing. These symptoms may suggest epiglottitis or a retropharyngeal abscess, which require immediate attention.

To determine the likelihood of a streptococcal infection and the need for antibiotic treatment, two scoring systems can be used: CENTOR and FeverPAIN. The CENTOR criteria include tonsillar exudate, tender anterior cervical lymphadenopathy or lymphadenitis, history of fever, and absence of cough. The FeverPAIN criteria include fever, purulence, rapid onset of symptoms, severely inflamed tonsils, and absence of cough or coryza. Based on the scores from these criteria, the likelihood of a streptococcal infection can be estimated, and appropriate management can be undertaken. can

Nasopharyngeal airway adjuncts (NPAs) are selected based on their length, which should match the distance between the nostril and the tragus of the ear.

Further Reading:

Techniques to keep the airway open:

1. Suction: Used to remove obstructing material such as blood, vomit, secretions, and food debris from the oral cavity.

2. Chin lift manoeuvres: Involves lifting the head off the floor and lifting the chin to extend the head in relation to the neck. Improves alignment of the pharyngeal, laryngeal, and oral axes.

3. Jaw thrust: Used in trauma patients with cervical spine injury concerns. Fingers are placed under the mandible and gently pushed upward.

Airway adjuncts:

1. Oropharyngeal airway (OPA): Prevents the tongue from occluding the airway. Sized according to the patient by measuring from the incisor teeth to the angle of the mandible. Inserted with the tip facing backwards and rotated 180 degrees once it touches the back of the palate or oropharynx.

2. Nasopharyngeal airway (NPA): Useful when it is difficult to open the mouth or in semi-conscious patients. Sized by length (distance between nostril and tragus of the ear) and diameter (roughly that of the patient’s little finger). Contraindicated in basal skull and midface fractures.

Laryngeal mask airway (LMA):

– Supraglottic airway device used as a first line or rescue airway.
– Easy to insert, sized according to patient’s bodyweight.
– Advantages: Easy insertion, effective ventilation, some protection from aspiration.
– Disadvantages: Risk of hypoventilation, greater gastric inflation than endotracheal tube (ETT), risk of aspiration and laryngospasm.

Note: Proper training and assessment of the patient’s condition are essential for airway management.

BPPV is a condition where patients experience vertigo and nystagmus. The Dix-Hallpike test is used to diagnose BPPV, and it involves observing torsional (rotary) and vertical nystagmus. Unlike vertigo caused by vestibular neuritis and labyrinthitis, BPPV is not associated with prodromal viral illness, hearing loss, or tinnitus. The episodes of vertigo and dizziness in BPPV usually last for 10-20 seconds, with episodes lasting over 1 minute being uncommon.

Further Reading:

Benign paroxysmal positional vertigo (BPPV) is a common cause of vertigo, characterized by sudden dizziness and vertigo triggered by changes in head position. It typically affects individuals over the age of 55 and is less common in younger patients. BPPV is caused by dysfunction in the inner ear, specifically the detachment of otoliths (calcium carbonate particles) from the utricular otolithic membrane. These loose otoliths move through the semicircular canals, triggering a sensation of movement and resulting in conflicting sensory inputs that cause vertigo.

The majority of BPPV cases involve otoliths in the posterior semicircular canal, followed by the inferior semicircular canal. BPPV in the anterior semicircular canals is rare. Clinical features of BPPV include vertigo triggered by head position changes, such as rolling over in bed or looking upwards, accompanied by nausea. Episodes of vertigo typically last 10-20 seconds and can be diagnosed through positional nystagmus, which is a specific eye movement, observed during diagnostic maneuvers like the Dix-Hallpike maneuver.

Hearing loss and tinnitus are not associated with BPPV. The prognosis for BPPV is generally good, with spontaneous resolution occurring within a few weeks to months. Symptomatic relief can be achieved through the Epley maneuver, which is successful in around 80% of cases, or patient home exercises like the Brandt-Daroff exercises. Medications like Betahistine may be prescribed but have limited effectiveness in treating BPPV.

Beta-blockers, like bisoprolol, and verapamil have a strong negative effect on the force of ventricular contraction. When these medications are taken together, they can significantly reduce ventricular contraction and lead to a slow heart rate, known as bradycardia. Additionally, the risk of developing AV block is increased. In certain situations, this combination can result in severe low blood pressure or even a complete absence of heart rhythm, known as asystole. Therefore, it is important to avoid using these medications together to prevent these potentially dangerous effects.

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.

Corneal microdeposits are found in almost all individuals (over 90%) who have been taking amiodarone for more than six months, particularly at doses higher than 400 mg/day. These deposits generally do not cause any symptoms, although approximately 10% of patients may experience a perception of a ‘bluish halo’ around objects they see.

Amiodarone can also have other effects on the eye, but these are much less common, occurring in only 1-2% of patients. These effects include optic neuropathy, nonarteritic anterior ischemic optic neuropathy (N-AION), optic disc swelling, and visual field defects.

The clinical symptoms of mitral stenosis include shortness of breath, which tends to worsen during exercise and when lying flat. Tiredness, palpitations, ankle swelling, cough, and haemoptysis are also common symptoms. Chest discomfort is rarely reported.

The clinical signs of mitral stenosis can include a malar flush, an irregular pulse if atrial fibrillation is present, a tapping apex beat that can be felt as the first heart sound, and a left parasternal heave if there is pulmonary hypertension. The first heart sound is often loud, and a mid-diastolic murmur can be heard best at the apex in the left lateral position during expiration using the bell of the stethoscope.

Mitral stenosis is typically caused by rheumatic heart disease, with about two-thirds of patients being female. During pregnancy, the increase in plasma volume can lead to elevated left atrial and pulmonary venous pressures. This can exacerbate any symptoms related to mitral stenosis and potentially result in pulmonary edema, as seen in this case.

Early assessment of the airway is a critical aspect of managing a burned patient. Airway obstruction can occur rapidly due to direct injury or swelling from the burn. If there is a history of trauma, the airway should be evaluated while maintaining cervical spine control.

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

In cases where significant swelling is anticipated, it may be necessary to urgently secure the airway with an uncut endotracheal tube before the swelling becomes severe. Delaying recognition of impending airway obstruction can make intubation difficult, and a surgical airway may be required.

The American Burn Life Support (ABLS) guidelines recommend early intubation in certain situations. These include signs of airway obstruction, extensive burns, deep facial burns, burns inside the mouth, significant swelling or risk of swelling, difficulty swallowing, respiratory compromise, decreased level of consciousness, and anticipated transfer of a patient with a large burn and airway issues without qualified personnel to intubate during transport.

Circumferential burns of the neck can cause tissue swelling around the airway, making early intubation necessary in these cases as well.

Calcium-channel blocker overdose is a serious matter and should always be treated as potentially life-threatening. The two most dangerous types of calcium channel blockers in overdose are verapamil and diltiazem. These medications work by binding to the alpha-1 subunit of L-type calcium channels, which prevents the entry of calcium into cells. These channels play a crucial role in the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

The toxic effects of calcium-channel blockers can be summarized as follows:

Cardiac effects:
– Excessive negative inotropy: causing myocardial depression
– Negative chronotropy: leading to sinus bradycardia
– Negative dromotropy: resulting in atrioventricular node blockade

Vascular smooth muscle tone effects:
– Decreased afterload: causing systemic hypotension
– Coronary vasodilation: leading to widened blood vessels in the heart

Metabolic effects:
– Hypoinsulinaemia: insulin release depends on calcium influx through L-type calcium channels in islet beta-cells
– Calcium channel blocker-induced insulin resistance: causing reduced responsiveness to insulin.

It is important to be aware of these effects and take appropriate action in cases of calcium-channel blocker overdose.

The normal intracranial pressure (ICP) for an adult lying down is typically between 5 and 15 mmHg.

Further Reading:

Intracranial pressure (ICP) refers to the pressure within the craniospinal compartment, which includes neural tissue, blood, and cerebrospinal fluid (CSF). Normal ICP for a supine adult is 5-15 mmHg. The body maintains ICP within a narrow range through shifts in CSF production and absorption. If ICP rises, it can lead to decreased cerebral perfusion pressure, resulting in cerebral hypoperfusion, ischemia, and potentially brain herniation.

The cranium, which houses the brain, is a closed rigid box in adults and cannot expand. It is made up of 8 bones and contains three main components: brain tissue, cerebral blood, and CSF. Brain tissue accounts for about 80% of the intracranial volume, while CSF and blood each account for about 10%. The Monro-Kellie doctrine states that the sum of intracranial volumes is constant, so an increase in one component must be offset by a decrease in the others.

There are various causes of raised ICP, including hematomas, neoplasms, brain abscesses, edema, CSF circulation disorders, venous sinus obstruction, and accelerated hypertension. Symptoms of raised ICP include headache, vomiting, pupillary changes, reduced cognition and consciousness, neurological signs, abnormal fundoscopy, cranial nerve palsy, hemiparesis, bradycardia, high blood pressure, irregular breathing, focal neurological deficits, seizures, stupor, coma, and death.

Measuring ICP typically requires invasive procedures, such as inserting a sensor through the skull. Management of raised ICP involves a multi-faceted approach, including antipyretics to maintain normothermia, seizure control, positioning the patient with a 30º head up tilt, maintaining normal blood pressure, providing analgesia, using drugs to lower ICP (such as mannitol or saline), and inducing hypocapnoeic vasoconstriction through hyperventilation. If these measures are ineffective, second-line therapies like barbiturate coma, optimised hyperventilation, controlled hypothermia, or decompressive craniectomy may be considered.

HbAS is known as Sickle cell trait, while HbSS is the genotype for Sickle-cell disease. Sickle-shaped red blood cells have a shorter lifespan of 10-20 days compared to the normal red blood cells that live for 90-120 days. Cholelithiasis, a complication of sickle-cell disease, occurs due to excessive bilirubin production caused by the breakdown of red blood cells. The inheritance pattern of sickle-cell disease is autosomal recessive. The disease is caused by a point mutation in the beta-globin chain of hemoglobin, resulting in the substitution of glutamic acid with valine at the sixth position. Individuals with one normal hemoglobin gene and one sickle gene have the genotype HbAS, which is commonly referred to as Sickle Cell trait.

After the third shock is administered to patients with a shockable rhythm, it is recommended to administer two drugs: adrenaline and amiodarone. Adrenaline should be given at a dose of 1 mg intravenously (or intraosseously) for adult patients in cardiac arrest with a shockable rhythm. For adult patients in cardiac arrest who are in ventricular fibrillation or pulseless ventricular tachycardia, amiodarone should be given at a dose of 300 mg intravenously (or intraosseously) after three shocks have been administered. In cases where amiodarone is unavailable, lidocaine may be used as an alternative.

Further Reading:

Cardiopulmonary arrest is a serious event with low survival rates. In non-traumatic cardiac arrest, only about 20% of patients who arrest as an in-patient survive to hospital discharge, while the survival rate for out-of-hospital cardiac arrest is approximately 8%. The Resus Council BLS/AED Algorithm for 2015 recommends chest compressions at a rate of 100-120 per minute with a compression depth of 5-6 cm. The ratio of chest compressions to rescue breaths is 30:2.

After a cardiac arrest, the goal of patient care is to minimize the impact of post cardiac arrest syndrome, which includes brain injury, myocardial dysfunction, the ischaemic/reperfusion response, and the underlying pathology that caused the arrest. The ABCDE approach is used for clinical assessment and general management. Intubation may be necessary if the airway cannot be maintained by simple measures or if it is immediately threatened. Controlled ventilation is aimed at maintaining oxygen saturation levels between 94-98% and normocarbia. Fluid status may be difficult to judge, but a target mean arterial pressure (MAP) between 65 and 100 mmHg is recommended. Inotropes may be administered to maintain blood pressure. Sedation should be adequate to gain control of ventilation, and short-acting sedating agents like propofol are preferred. Blood glucose levels should be maintained below 8 mmol/l. Pyrexia should be avoided, and there is some evidence for controlled mild hypothermia but no consensus on this.

Post ROSC investigations may include a chest X-ray, ECG monitoring, serial potassium and lactate measurements, and other imaging modalities like ultrasonography, echocardiography, CTPA, and CT head, depending on availability and skills in the local department. Treatment should be directed towards the underlying cause, and PCI or thrombolysis may be considered for acute coronary syndrome or suspected pulmonary embolism, respectively.

Patients who are comatose after ROSC without significant pre-arrest comorbidities should be transferred to the ICU for supportive care. Neurological outcome at 72 hours is the best prognostic indicator of outcome.

Haloperidol should not be used in patients with Parkinson’s, Lewy body dementia, or prolonged QT syndrome. It is the first choice for controlling aggressive behavior in most patients with delirium, but lorazepam is preferred for patients with Parkinson’s, Lewy body dementia, prolonged QT syndrome, extrapyramidal side effects, or delirium due to alcohol withdrawal. Haloperidol can reduce the effectiveness of levodopa in Parkinson’s disease by blocking dopamine receptors in the corpus striatum, which can lead to worsened motor function, psychosis, or a combination of both.

Further Reading:

Delirium is an acute syndrome that causes disturbances in consciousness, attention, cognition, and perception. It is also known as an acute confusional state. The DSM-IV criteria for diagnosing delirium include recent onset of fluctuating awareness, impairment of memory and attention, and disorganized thinking. Delirium typically develops over hours to days and may be accompanied by behavioral changes, personality changes, and psychotic features. It often occurs in individuals with predisposing factors, such as advanced age or multiple comorbidities, when exposed to new precipitating factors, such as medications or infection. Symptoms of delirium fluctuate throughout the day, with lucid intervals occurring during the day and worse disturbances at night. Falling and loss of appetite are often warning signs of delirium.

Delirium can be classified into three subtypes based on the person’s symptoms. Hyperactive delirium is characterized by inappropriate behavior, hallucinations, and agitation. Restlessness and wandering are common in this subtype. Hypoactive delirium is characterized by lethargy, reduced concentration, and appetite. The person may appear quiet or withdrawn. Mixed delirium presents with signs and symptoms of both hyperactive and hypoactive subtypes.

The exact pathophysiology of delirium is not fully understood, but it is believed to involve multiple mechanisms, including cholinergic deficiency, dopaminergic excess, and inflammation. The cause of delirium is usually multifactorial, with predisposing factors and precipitating factors playing a role. Predisposing factors include older age, cognitive impairment, frailty, significant injuries, and iatrogenic events. Precipitating factors include infection, metabolic or electrolyte disturbances, cardiovascular disorders, respiratory disorders, neurological disorders, endocrine disorders, urological disorders, gastrointestinal disorders, severe uncontrolled pain, alcohol intoxication or withdrawal, medication use, and psychosocial factors.

Delirium is highly prevalent in hospital settings, affecting up to 50% of inpatients aged over 65 and occurring in 30% of people aged over 65 presenting to the emergency department. Complications of delirium include increased risk of death, high in-hospital mortality rates, higher mortality rates following hospital discharge, increased length of stay in hospital, nosocomial infections, increased risk of admission to long-term care or re-admission to hospital, increased incidence of dementia, increased risk of falls and associated injuries and pressure sores.

First-generation antipsychotics, also known as conventional or typical antipsychotics, are powerful blockers of the dopamine D2 receptor. However, each drug in this category has different effects on other receptors, such as serotonin type 2 (5-HT2), alpha1, histaminic, and muscarinic receptors.

These first-generation antipsychotics are known to have a high incidence of extrapyramidal side effects, which include rigidity, bradykinesia, dystonias, tremor, akathisia, tardive dyskinesia, and neuroleptic malignant syndrome (NMS). NMS is a rare and life-threatening reaction to neuroleptic medications, characterized by fever, muscle stiffness, changes in mental state, and dysfunction of the autonomic nervous system. NMS typically occurs shortly after starting or increasing the dose of neuroleptic treatment.

On the other hand, second-generation antipsychotics, also referred to as novel or atypical antipsychotics, are dopamine D2 antagonists, except for aripiprazole. These medications are associated with lower rates of extrapyramidal side effects and NMS compared to the first-generation antipsychotics. However, they have higher rates of metabolic side effects and weight gain.

It is important to note that serotonin syndrome shares similar features with NMS but can be distinguished by the causative agent, most commonly the serotonin-specific reuptake inhibitors.