First-generation antipsychotics, also known as conventional or typical antipsychotics, are potent blockers of dopamine D2 receptors. However, these drugs also have varying effects on other receptors such as serotonin type 2 (5-HT2), alpha1, histaminic, and muscarinic receptors.

One of the major drawbacks of first-generation antipsychotics is their high incidence of extrapyramidal side effects. These include rigidity, bradykinesia, dystonias, tremor, akathisia, and tardive dyskinesia. Additionally, there is a rare but life-threatening reaction called neuroleptic malignant syndrome (NMS) that can occur with these medications. NMS is characterized by fever, muscle rigidity, altered mental status, and autonomic dysfunction. It typically occurs shortly after starting or increasing the dose of a neuroleptic medication.

In contrast, second-generation antipsychotics, also known as novel or atypical antipsychotics, have a lower risk of extrapyramidal side effects and NMS compared to their first-generation counterparts. However, they are associated with higher rates of metabolic effects and weight gain.

It is important to differentiate serotonin syndrome from NMS as they share similar features. Serotonin syndrome is most commonly caused by serotonin-specific reuptake inhibitors.

Here are some commonly encountered examples of first- and second-generation antipsychotics:

First-generation:
– Chlopromazine
– Haloperidol
– Fluphenazine
– Trifluoperazine

Second-generation:
– Clozapine
– Olanzapine
– Quetiapine
– Risperidone
– Aripiprazole

Transfusion transmitted bacterial infection is a rare complication that can occur during blood transfusion. It is more commonly associated with platelet transfusion, as platelets are stored at room temperature. Additionally, previously frozen components that are thawed using a water bath and red cell components stored for several weeks are also at a higher risk for bacterial infection.

Both Gram-positive and Gram-negative bacteria have been implicated in transfusion-transmitted bacterial infection, but Gram-negative bacteria are known to cause more severe illness and have higher rates of morbidity and mortality. Among the bacterial organisms, Yersinia enterocolitica is the most commonly associated with this type of infection. This particular organism is able to multiply at low temperatures and utilizes iron as a nutrient, making it well-suited for proliferation in blood stores.

The clinical features of transfusion-transmitted bacterial infection typically manifest shortly after the transfusion begins. These features include a high fever, chills and rigors, nausea and vomiting, tachycardia, hypotension, and even circulatory collapse.

If there is suspicion of a transfusion-transmitted bacterial infection, it is crucial to immediately stop the transfusion. Blood cultures and a Gram-stain should be requested to identify the specific bacteria causing the infection. Broad-spectrum antibiotics should be initiated promptly. Furthermore, the blood pack should be returned to the blood bank urgently for culture and Gram-stain analysis.

The type of consent in this scenario is implied consent. Implied consent is when a patient’s actions or behavior indicate their agreement to a medical procedure or treatment. In this case, the patient nodding in agreement to receive a local anesthetic injection implies their consent for the procedure.

Further Reading:

Patients have the right to determine what happens to their own bodies, and for consent to be valid, certain criteria must be met. These criteria include the person being informed about the intervention, having the capacity to consent, and giving consent voluntarily and freely without any pressure or undue influence.

In order for a person to be deemed to have capacity to make a decision on a medical intervention, they must be able to understand the decision and the information provided, retain that information, weigh up the pros and cons, and communicate their decision.

Valid consent can only be provided by adults, either by the patient themselves, a person authorized under a Lasting Power of Attorney, or someone with the authority to make treatment decisions, such as a court-appointed deputy or a guardian with welfare powers.

In the UK, patients aged 16 and over are assumed to have the capacity to consent. If a patient is under 18 and appears to lack capacity, parental consent may be accepted. However, a young person of any age may consent to treatment if they are considered competent to make the decision, known as Gillick competence. Parental consent may also be given by those with parental responsibility.

The Fraser guidelines apply to the prescription of contraception to under 16’s without parental involvement. These guidelines allow doctors to provide contraceptive advice and treatment without parental consent if certain criteria are met, including the young person understanding the advice, being unable to be persuaded to inform their parents, and their best interests requiring them to receive contraceptive advice or treatment.

Competent adults have the right to refuse consent, even if it is deemed unwise or likely to result in harm. However, there are exceptions to this, such as compulsory treatment authorized by the mental health act or if the patient is under 18 and refusing treatment would put their health at serious risk.

In emergency situations where a patient is unable to give consent, treatment may be provided without consent if it is immediately necessary to save their life or prevent a serious deterioration of their condition. Any treatment decision made without consent must be in the patient’s best interests, and if a decision is time-critical and the patient is unlikely to regain capacity in time, a best interest decision should be made. The treatment provided should be the least restrictive on the patient’s future choices.

This patient is displaying symptoms that are characteristic of normal-pressure hydrocephalus (NPH). NPH is a type of communicating hydrocephalus where the pressure inside the skull, as measured through a lumbar puncture, is either normal or occasionally elevated. It primarily affects elderly individuals, and the likelihood of developing NPH increases with age.

Around 50% of NPH cases are considered idiopathic, meaning there is no identifiable cause. The remaining cases are secondary to various conditions such as head injury, meningitis, subarachnoid hemorrhage, central nervous system tumors, and radiotherapy.

The typical presentation of NPH includes a classic triad of symptoms: gait disturbance (often characterized by a broad-based and shuffling gait), sphincter disturbance leading to incontinence (usually urinary incontinence), and progressive dementia with memory loss, inattention, inertia, and bradyphrenia.

Diagnosing NPH primarily relies on identifying the classic clinical triad mentioned above. Additional investigations can provide supportive evidence, including CT and MRI scans that reveal enlarged ventricles and periventricular lucency. Lumbar puncture may also be performed, with the cerebrospinal fluid (CSF) typically appearing normal or intermittently elevated. Intraventricular monitoring may show beta waves for more than 5% of a 24-hour period.

NPH is one of the few reversible causes of dementia, making early recognition and treatment crucial. Medical treatment options such as carbonic anhydrase inhibitors (e.g., acetazolamide) and repeated lumbar punctures can provide temporary relief. However, the definitive treatment for NPH involves surgically inserting a cerebrospinal fluid (CSF) shunt. This procedure has shown lasting clinical benefits in 70% to 90% of patients compared to their pre-operative state.

An open pneumothorax, also known as a sucking chest wound, occurs when air enters the pleural space due to an open chest wound or physical defect. This can lead to ineffective ventilation, causing hypoxia and hypercarbia. Air can enter the pleural cavity passively or be sucked in during inspiration, leading to lung collapse on that side. Sucking wounds can be heard audibly as air passes through the chest defect, and entry wounds are usually visible.

To manage an open pneumothorax, respiratory compromise can be alleviated by covering the wound with a dressing or using a chest seal device. It is important to ensure that one side of the dressing is not occluded, allowing the dressing to function as a flutter valve and prevent significant air ingress during inspiration while allowing air to escape the pleural cavity. If tension pneumothorax is suspected after applying a dressing, the dressing may need to be temporarily removed for decompression.

Intubation and intermittent positive pressure ventilation (IPPV) can be used to ventilate the patient and alleviate respiratory distress. Definitive management involves either inserting a chest drain or surgically repairing the defect. Surgical repair is typically preferred, especially for large wounds.

This patient is experiencing an increased heart rate and respiratory rate, as well as a decrease in urine output. Additionally, they are feeling anxious and confused. These symptoms indicate that the patient has suffered a class III haemorrhage at this point in time.

Recognizing the extent of blood loss based on vital signs and mental status abnormalities is a crucial skill. The Advanced Trauma Life Support (ATLS) haemorrhagic shock classification connects the amount of blood loss to expected physiological responses in a healthy 70 kg patient. In a 70 kg male patient, the total circulating blood volume is approximately five liters, which accounts for about 7% of their total body weight.

The ATLS haemorrhagic shock classification is summarized as follows:

CLASS I:
– Blood loss: Up to 750 mL
– Blood loss (% blood volume): Up to 15%
– Pulse rate: Less than 100 bpm
– Systolic BP: Normal
– Pulse pressure: Normal (or increased)
– Respiratory rate: 14-20 breaths per minute
– Urine output: Greater than 30 mL/hr
– CNS/mental status: Slightly anxious

CLASS II:
– Blood loss: 750-1500 mL
– Blood loss (% blood volume): 15-30%
– Pulse rate: 100-120 bpm
– Systolic BP: Normal
– Pulse pressure: Decreased
– Respiratory rate: 20-30 breaths per minute
– Urine output: 20-30 mL/hr
– CNS/mental status: Mildly anxious

CLASS III:
– Blood loss: 1500-2000 mL
– Blood loss (% blood volume): 30-40%
– Pulse rate: 120-140 bpm
– Systolic BP: Decreased
– Pulse pressure: Decreased
– Respiratory rate: 30-40 breaths per minute
– Urine output: 5-15 mL/hr
– CNS/mental status: Anxious, confused

CLASS IV:
– Blood loss: More than 2000 mL
– Blood loss (% blood volume): More than 40%
– Pulse rate: More than 140 bpm
– Systolic BP: Decreased
– Pulse pressure: Decreased
– Respiratory rate: More than 40 breaths per minute
– Urine output: Negligible
– CNS/mental status: Confused, leth

Compartment syndrome can occur when there are circumferential burns on the arms or legs. This typically happens with full thickness burns, where the burnt skin becomes stiff and compresses the compartment, making it difficult for blood to flow out. To treat this condition, escharotomy and possibly fasciotomy may be necessary.

Further Reading:

Burn injuries can be classified based on their type (degree, partial thickness or full thickness), extent as a percentage of total body surface area (TBSA), and severity (minor, moderate, major/severe). Severe burns are defined as a >10% TBSA in a child and >15% TBSA in an adult.

When assessing a burn, it is important to consider airway injury, carbon monoxide poisoning, type of burn, extent of burn, special considerations, and fluid status. Special considerations may include head and neck burns, circumferential burns, thorax burns, electrical burns, hand burns, and burns to the genitalia.

Airway management is a priority in burn injuries. Inhalation of hot particles can cause damage to the respiratory epithelium and lead to airway compromise. Signs of inhalation injury include visible burns or erythema to the face, soot around the nostrils and mouth, burnt/singed nasal hairs, hoarse voice, wheeze or stridor, swollen tissues in the mouth or nostrils, and tachypnea and tachycardia. Supplemental oxygen should be provided, and endotracheal intubation may be necessary if there is airway obstruction or impending obstruction.

The initial management of a patient with burn injuries involves conserving body heat, covering burns with clean or sterile coverings, establishing IV access, providing pain relief, initiating fluid resuscitation, measuring urinary output with a catheter, maintaining nil by mouth status, closely monitoring vital signs and urine output, monitoring the airway, preparing for surgery if necessary, and administering medications.

Burns can be classified based on the depth of injury, ranging from simple erythema to full thickness burns that penetrate into subcutaneous tissue. The extent of a burn can be estimated using methods such as the rule of nines or the Lund and Browder chart, which takes into account age-specific body proportions.

Fluid management is crucial in burn injuries due to significant fluid losses. Evaporative fluid loss from burnt skin and increased permeability of blood vessels can lead to reduced intravascular volume and tissue perfusion. Fluid resuscitation should be aggressive in severe burns, while burns <15% in adults and <10% in children may not require immediate fluid resuscitation. The Parkland formula can be used to calculate the intravenous fluid requirements for someone with a significant burn injury.

Multiple sclerosis (MS) is a condition characterized by the demyelination of nerve cells in the brain and spinal cord. It is an autoimmune disease caused by recurring inflammation, primarily affecting individuals in early adulthood. The ratio of affected females to males is 3:2.

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

MS can present in three main patterns. The most common is relapsing and remitting MS, characterized by periods of no symptoms followed by relapses (present in 80% of patients at diagnosis). Primary progressive MS is less common, with symptoms developing and worsening from the beginning and few remissions (present in 10-15% of patients at diagnosis). Secondary progressive MS follows relapsing/remitting MS, with worsening symptoms and fewer remissions (approximately 50% of those with relapsing/remitting MS will develop this within 10 years of diagnosis). Progressive relapsing MS is rare and involves a steady decline in neurological function from the onset of the disease, with superimposed attacks also occurring.

Certain factors can indicate a more favorable prognosis for individuals with MS. These include having a relapsing/remitting course, being female, experiencing sensory symptoms, and having an early age at onset.

Eye movement desensitization and reprocessing (EMDR) and trauma-focused cognitive-behavioral therapy (CBT) are the primary treatment options for post-traumatic stress disorder (PTSD). These therapies should be provided to individuals of all ages, including children, adolescents, and adults, regardless of the time that has passed since the traumatic event. The recommended number of sessions is typically 8-12, although additional sessions may be necessary in cases involving multiple traumas, chronic disability, comorbidities, or social difficulties.

Macrolide antibiotics, such as clarithromycin and erythromycin, are widely known to prolong the International Normalized Ratio (INR). Several drugs can increase the potency of warfarin, and the macrolides, along with ciprofloxacin and metronidazole, are the antibiotics that have the most significant impact on enhancing the effect of warfarin.

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 size of an oropharyngeal airway (OPA or Guedel) can be determined by measuring the distance between the patient’s incisors and the angle of their mandible. To ensure proper fit, the OPA should be approximately the same length as this measurement. Please refer to the image in the notes for visual guidance.

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.

Methicillin-resistant Staphylococcus aureus (MRSA) has become a significant issue in hospitals and other healthcare facilities in recent years. MRSA refers to any strain of Staphylococcus aureus that has developed resistance to beta-lactam antibiotics, such as penicillins and cephalosporins. This resistance is caused by the presence of the mecA gene, which produces a penicillin-binding protein with low affinity. Fortunately, MRSA is typically susceptible to teicoplanin, vancomycin, daptomycin, and linezolid. On the other hand, imipenem is an intravenous beta-lactam antibiotic that belongs to the carbapenem subgroup.

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.

Glanzmann’s thrombasthenia is an uncommon condition affecting platelets, where they have a deficiency or abnormality in glycoprotein IIb/IIIa. This disorder leads to platelet dysfunction and can result in various complications.

The most common symptom of infective endocarditis is fever, which occurs in the majority of cases and is consistently present throughout the course of the disease. Cardiac murmurs are also frequently detected, although they may only be present in one third of patients at the initial presentation. Individuals who use intravenous drugs often develop right-sided disease affecting the tricuspid and pulmonary valves, making it challenging to detect cardiac murmurs in these cases. Splinter hemorrhages and other symptoms may also be observed.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

This patient has come in with worsening breathlessness and coughing, along with coughing up blood, all of which are occurring on top of their existing lung cancer. The diagnosis in this case is superior vena cava obstruction, which is being caused by the primary bronchial neoplasm.

The typical clinical presentation of superior vena cava obstruction includes breathlessness and coughing, chest pain, swelling in the neck, face, and arms, dilated veins and telangiectasia on the arms, neck, and chest wall, facial flushing, stridor due to laryngeal edema, and cyanosis.

Given the urgency of the situation, this man will require immediate treatment. Upon initial presentation, it is important to elevate his head and provide supplemental oxygen to alleviate symptoms. Additionally, corticosteroids and diuretics may be administered. Further investigation will be necessary through CT scanning, and radiotherapy may be recommended as a potential course of action.

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

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

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

The current algorithm for the treatment of a convulsing child, known as APLS, is as follows:

Step 1 (5 minutes after the start of convulsion):
If a child has been convulsing for 5 minutes or more, the initial dose of benzodiazepine should be administered. This can be done by giving Lorazepam at a dose of 0.1 mg/kg intravenously (IV) or intraosseously (IO) if vascular access is available. Alternatively, buccal midazolam at a dose of 0.5 mg/kg or rectal diazepam at a dose of 0.5 mg/kg can be given if vascular access is not available.

Step 2 (10 minutes after the start of Step 1):
If the convulsion continues for a further 10 minutes, a second dose of benzodiazepine should be given. It is also important to summon senior help at this point.

Step 3 (10 minutes after the start of Step 2):
At this stage, it is necessary to involve senior help to reassess the child and provide guidance on further management. The recommended approach is as follows:
– If the child is not already on phenytoin, a phenytoin infusion should be initiated. This involves administering 20 mg/kg of phenytoin intravenously over a period of 20 minutes.
– If the child is already taking phenytoin, phenobarbitone can be used as an alternative. The recommended dose is 20 mg/kg administered intravenously over 20 minutes.
– In the meantime, rectal paraldehyde can be considered at a dose of 0.8 ml/kg of the 50:50 mixture while preparing the infusion.

Step 4 (20 minutes after the start of Step 3):
If the child is still experiencing convulsions at this stage, it is crucial to have an anaesthetist present. A rapid sequence induction with thiopental is recommended for further management.

Please note that this algorithm is subject to change based on individual patient circumstances and the guidance of medical professionals.

Addison’s disease, a condition characterized by insufficient production of hormones by the adrenal glands, has different causes depending on the geographical location. Tuberculosis is the leading cause of Addison’s disease globally, while autoimmune adrenalitis is the most common cause in developed countries like the UK.

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.

According to the current NICE guidelines on febrile illness in children under the age of 5, there are certain symptoms and signs that may indicate the presence of pneumonia. These include tachypnoea, which is a rapid breathing rate. For infants aged 0-5 months, a respiratory rate (RR) of over 60 breaths per minute is considered suggestive of pneumonia. For infants aged 6-12 months, an RR of over 50 breaths per minute is indicative, and for children older than 12 months, an RR of over 40 breaths per minute may suggest pneumonia.

Other signs that may point towards pneumonia include crackles in the chest, nasal flaring, chest indrawing, and cyanosis. Crackles are abnormal sounds heard during breathing, while nasal flaring refers to the widening of the nostrils during breathing. Chest indrawing is the inward movement of the chest wall during inhalation, and cyanosis is the bluish discoloration of the skin or mucous membranes due to inadequate oxygen supply.

Additionally, a low oxygen saturation level of less than 95% while breathing air is also considered suggestive of pneumonia. These guidelines can be found in more detail in the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

To remove contaminated material, it is recommended to remove and dispose of clothing. It is important to seal the clothing and treat it as hazardous waste. If wet decontamination is being utilized, patients should shower using warm water and detergent.

Further Reading:

Chemical incidents can occur as a result of leaks, spills, explosions, fires, terrorism, or the use of chemicals during wars. Industrial sites that use chemicals are required to conduct risk assessments and have accident plans in place for such incidents. Health services are responsible for decontamination, unless mass casualties are involved, and all acute health trusts must have major incident plans in place.

When responding to a chemical incident, hospitals prioritize containment of the incident and prevention of secondary contamination, triage with basic first aid, decontamination if not done at the scene, recognition and management of toxidromes (symptoms caused by exposure to specific toxins), appropriate supportive or antidotal treatment, transfer to definitive treatment, a safe end to the hospital response, and continuation of business after the event.

To obtain advice when dealing with chemical incidents, the two main bodies are Toxbase and the National Poisons Information Service. Signage on containers carrying chemicals and material safety data sheets (MSDS) accompanying chemicals also provide information on the chemical contents and their hazards.

Contamination in chemical incidents can occur in three phases: primary contamination from the initial incident, secondary contamination spread via contaminated people leaving the initial scene, and tertiary contamination spread to the environment, including becoming airborne and waterborne. The ideal personal protective equipment (PPE) for chemical incidents is an all-in-one chemical-resistant overall with integral head/visor and hands/feet worn with a mask, gloves, and boots.

Decontamination of contaminated individuals involves the removal and disposal of contaminated clothing, followed by either dry or wet decontamination. Dry decontamination is suitable for patients contaminated with non-caustic chemicals and involves blotting and rubbing exposed skin gently with dry absorbent material. Wet decontamination is suitable for patients contaminated with caustic chemicals and involves a warm water shower while cleaning the body with simple detergent.

After decontamination, the focus shifts to assessing the extent of any possible poisoning and managing it. The patient’s history should establish the chemical the patient was exposed to, the volume and concentration of the chemical, the route of exposure, any protective measures in place, and any treatment given. Most chemical poisonings require supportive care using standard resuscitation principles, while some chemicals have specific antidotes. Identifying toxidromes can be useful in guiding treatment, and specific antidotes may be administered accordingly.

NICE recommends considering admission for patients with acute diverticulitis if they experience pain that cannot be effectively controlled with paracetamol. Additionally, if a patient is unable to maintain hydration through oral fluids or cannot tolerate oral antibiotics, admission should be considered. Admission is also recommended for frail patients or those with significant comorbidities, particularly if they are immunosuppressed. Furthermore, admission should be considered if any of the following suspected complications arise: rectal bleeding requiring transfusion, perforation and peritonitis, intra-abdominal abscess, or fistula. Lastly, if symptoms persist after 48 hours despite conservative management at home, admission should be considered.

An overdose of aspirin often leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the stimulation of the respiratory center causes hyperventilation and results in respiratory alkalosis. However, as the overdose progresses, the direct acidic effects of aspirin cause an increase in the anion gap and metabolic acidosis.

Here is a summary of common causes for different acid-base disorders:

Respiratory alkalosis can be caused by hyperventilation due to factors such as anxiety, pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, and the early stages of aspirin overdose.

Respiratory acidosis can occur in individuals with chronic obstructive pulmonary disease (COPD), life-threatening asthma, pulmonary edema, sedative drug overdose (such as opioids or benzodiazepines), neuromuscular diseases, and obesity.

Metabolic alkalosis can be caused by vomiting, potassium depletion (often due to diuretic usage), Cushing’s syndrome, and Conn’s syndrome.

Metabolic acidosis with a raised anion gap can result from conditions such as lactic acidosis (caused by factors like hypoxemia, shock, sepsis, or tissue infarction), ketoacidosis (associated with diabetes, starvation, or excessive alcohol consumption), renal failure, and poisoning (including the late stages of aspirin overdose, methanol or ethylene glycol ingestion).

Metabolic acidosis with a normal anion gap can be seen in renal tubular acidosis, diarrhea, ammonium chloride ingestion, and adrenal insufficiency.

Septic arthritis occurs when an infectious agent invades a joint, causing it to become purulent. The main symptoms of septic arthritis include pain in the affected joint, redness, warmth, and swelling of the joint, and difficulty moving the joint. Patients may also experience fever and systemic upset. The most common cause of septic arthritis is Staphylococcus aureus, but other bacteria such as Streptococcus spp., Haemophilus influenzae, Neisseria gonorrhoea, and Escherichia coli can also be responsible.

According to the current recommendations by NICE and the BNF, the initial treatment for septic arthritis is flucloxacillin. However, if a patient is allergic to penicillin, clindamycin can be used instead. If there is a suspicion of MRSA infection, vancomycin is the recommended choice. In cases where gonococcal arthritis or a Gram-negative infection is suspected, cefotaxime is the preferred treatment. The suggested duration of treatment is typically 4-6 weeks, although it may be longer if the infection is complicated.

Placental abruption, also known as abruptio placentae, occurs when the placental lining separates from the wall of the uterus before delivery and after 20 weeks of gestation.

In the early stages, there may be no symptoms, but typically abdominal pain and vaginal bleeding develop. Approximately 20% of patients experience a concealed placental abruption, where the haemorrhage is confined within the uterine cavity and the amount of blood loss can be significantly underestimated.

The clinical features of placental abruption include sudden onset abdominal pain (which can be severe), variable vaginal bleeding, severe or continuous contractions, abdominal tenderness, and an enlarged, tense uterus. The foetus often shows signs of distress, such as reduced movements, increased or decreased fetal heart rate, decreased variability of fetal heart rate, and late decelerations.

In contrast, placenta praevia is painless and the foetal heart is generally normal. The degree of obstetric shock is usually proportional to the amount of vaginal blood loss. Another clue that the cause of bleeding is placenta praevia rather than placental abruption is that the foetus may have an abnormal presentation or lie.

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.

The secretion of aldosterone occurs in the zona glomerulosa of the adrenal cortex.

Further Reading:

Hyperaldosteronism is a condition characterized by excessive production of aldosterone by the adrenal glands. It can be classified into primary and secondary hyperaldosteronism. Primary hyperaldosteronism, also known as Conn’s syndrome, is typically caused by adrenal hyperplasia or adrenal tumors. Secondary hyperaldosteronism, on the other hand, is a result of high renin levels in response to reduced blood flow across the juxtaglomerular apparatus.

Aldosterone is the main mineralocorticoid steroid hormone produced by the adrenal cortex. It acts on the distal renal tubule and collecting duct of the nephron, promoting the reabsorption of sodium ions and water while secreting potassium ions.

The causes of hyperaldosteronism vary depending on whether it is primary or secondary. Primary hyperaldosteronism can be caused by adrenal adenoma, adrenal hyperplasia, adrenal carcinoma, or familial hyperaldosteronism. Secondary hyperaldosteronism can be caused by renal artery stenosis, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, or cor pulmonale.

Clinical features of hyperaldosteronism include hypertension, hypokalemia, metabolic alkalosis, hypernatremia, polyuria, polydipsia, headaches, lethargy, muscle weakness and spasms, and numbness. It is estimated that hyperaldosteronism is present in 5-10% of patients with hypertension, and hypertension in primary hyperaldosteronism is often resistant to drug treatment.

Diagnosis of hyperaldosteronism involves various investigations, including U&Es to assess electrolyte disturbances, aldosterone-to-renin plasma ratio (ARR) as the gold standard diagnostic test, ECG to detect arrhythmia, CT/MRI scans to locate adenoma, fludrocortisone suppression test or oral salt testing to confirm primary hyperaldosteronism, genetic testing to identify familial hyperaldosteronism, and adrenal venous sampling to determine lateralization prior to surgery.

Treatment of primary hyperaldosteronism typically involves surgical adrenalectomy for patients with unilateral primary aldosteronism. Diet modification with sodium restriction and potassium supplementation may also be recommended.

Thyroid storm, also known as thyrotoxic crisis, is a rare and dangerous complication of hyperthyroidism. The initial management of this condition involves the use of specific medications. These medications include a beta blocker, a corticosteroid, an antithyroid drug, and an iodine solution.

The beta blocker used is typically propranolol, which is administered intravenously at a dose of 1 mg over 1 minute. If a beta blocker is contraindicated, a calcium channel blocker such as diltiazem may be used instead, at a dose of 0.25 mg/kg over 2 minutes.

For corticosteroids, hydrocortisone is commonly used and given intravenously at a dose of 200 mg. Alternatively, dexamethasone can be used at a dose of 2 mg intravenously.

The antithyroid drug used is usually propylthiouracil, which is given orally, through a nasogastric tube, or rectally, at a dose of 200 mg.

An iodine solution, specifically Lugol’s iodine, is also part of the initial management. However, it should not be administered until at least 1 hour after the antithyroid drug has been given. This is because iodine can exacerbate thyrotoxicosis by stimulating thyroid hormone synthesis. Propylthiouracil, on the other hand, inhibits the normal interactions of iodine and peroxidase with thyroglobulin, preventing the formation of T4 and T3. Therefore, it is given first and allowed time to take effect before iodine is administered.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

High Altitude Cerebral Edema (HACE) is a condition that develops from acute mountain sickness (AMS). Ataxia, which refers to a lack of coordination, is the primary early indication of HACE. The mentioned symptoms are typical characteristics 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.

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

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

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

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