The use of NSAIDs during the third trimester of pregnancy is associated with several risks. These risks include delayed onset of labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus, which is a condition characterized by bilirubin-induced brain dysfunction. Additionally, there is a slight increase in the risk of first-trimester abortion if NSAIDs are used early in pregnancy.

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

Drug: ACE inhibitors (e.g. ramipril)
Adverse effects: If given in the second and third trimester, ACE inhibitors can cause hypoperfusion, renal failure, and the oligohydramnios sequence.

Drug: Aminoglycosides (e.g. gentamicin)
Adverse effects: Aminoglycosides can cause ototoxicity, leading to deafness in the fetus.

Drug: Aspirin
Adverse effects: High doses of aspirin can cause first-trimester abortions, delayed onset of labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g. 75 mg) have no significant associated risk.

Drug: Benzodiazepines (e.g. diazepam)
Adverse effects: When given late in pregnancy, benzodiazepines can cause respiratory depression and a neonatal withdrawal syndrome.

Drug: Calcium-channel blockers
Adverse effects: If given in the first trimester, calcium-channel blockers can cause phalangeal abnormalities. If given in the second and third trimester, they can cause fetal growth retardation.

Subdural hematoma (SDH) occurs when the bridging veins in the cortex of the brain tear and cause bleeding in the space between the brain and the outermost protective layer. This is different from extradural hematoma (EDH), which is usually caused by a rupture in the middle meningeal artery.

Further Reading:

A subdural hematoma (SDH) is a condition where there is a collection of blood between the dura mater and the arachnoid mater of the brain. It occurs when the cortical bridging veins tear and bleed into the subdural space. Risk factors for SDH include head trauma, cerebral atrophy, advancing age, alcohol misuse, and certain medications or bleeding disorders. SDH can be classified as acute, subacute, or chronic depending on its age or speed of onset. Acute SDH is typically the result of head trauma and can progress to become chronic if left untreated.

The clinical presentation of SDH can vary depending on the nature of the condition. In acute SDH, patients may initially feel well after a head injury but develop more serious neurological symptoms later on. Chronic SDH may be detected after a CT scan is ordered to investigate confusion or cognitive decline. Symptoms of SDH can include increasing confusion, progressive decline in neurological function, seizures, headache, loss of consciousness, and even death.

Management of SDH involves an ABCDE approach, seizure management, confirming the diagnosis with CT or MRI, checking clotting and correcting coagulation abnormalities, managing raised intracranial pressure, and seeking neurosurgical opinion. Some SDHs may be managed conservatively if they are small, chronic, the patient is not a good surgical candidate, and there are no neurological symptoms. Neurosurgical intervention typically involves a burr hole craniotomy to decompress the hematoma. In severe cases with high intracranial pressure and significant brain swelling, a craniectomy may be performed, where a larger section of the skull is removed and replaced in a separate cranioplasty procedure.

CT imaging can help differentiate between subdural hematoma and other conditions like extradural hematoma. SDH appears as a crescent-shaped lesion on CT scans.

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

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

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

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

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

The most probable diagnosis in this case is a subarachnoid haemorrhage (SAH).

When assessing patients who present with an SAH, they may exhibit focal neurological signs, which can indicate the potential location of the aneurysm. Common areas where aneurysms occur include the bifurcation of the middle cerebral artery, the junction of the anterior communicating cerebral artery, and the junction of the posterior communicating artery with the internal carotid artery. If there is complete or partial paralysis of the oculomotor nerve, it suggests the rupture of a posterior communicating artery aneurysm.

While hypertension is a risk factor for SAH, a significant increase in blood pressure may occur as a reflex response following the haemorrhage.

The recommended target SpO2, which measures the percentage of oxygen saturation in the blood, following a cardiac arrest is 94-98%. This range ensures that the patient receives adequate oxygenation without the risk of hyperoxia, which is an excess of oxygen in the body.

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.

Vestibular neuritis is a common complication of vestibular neuronitis, characterized by a following of people experiencing symptoms such as persistent dizziness, unsteadiness, and fear of falling. However, a rare complication called phobic postural vertigo may also occur, where individuals experience these symptoms despite not actually falling.

On the other hand, benign paroxysmal positional vertigo (BPPV) presents with short episodes of vertigo, usually lasting less than 20 seconds, triggered by changes in head position. In contrast, vestibular neuronitis causes constant vertigo, even when at rest, which can be worsened by head movements.

Recovery from vestibular neuronitis is a gradual process that typically takes a few weeks, up to 6 weeks. It is believed that this condition is caused by inflammation of the vestibular nerve following a viral infection. On the other hand, BPPV is thought to occur due to the presence of cellular debris or crystal formation in the semicircular canals.

Further Reading:

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

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

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

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

A massive haemothorax occurs when more than 1500 mL of blood, which is about 1/3 of the patient’s blood volume, rapidly accumulates in the chest cavity. The classic signs of a massive haemothorax include decreased chest expansion, decreased breath sounds, and dullness to percussion. Both tension pneumothorax and massive haemothorax can cause decreased breath sounds, but they can be differentiated through percussion. Hyperresonance indicates tension pneumothorax, while dullness suggests a massive haemothorax.

The first step in managing a massive haemothorax is to simultaneously restore blood volume and decompress the chest cavity by inserting a chest drain. In most cases, the bleeding in a haemothorax has already stopped by the time management begins, and simple drainage is sufficient. It is important to use a chest drain of adequate size (preferably 36F) to ensure effective drainage of the haemothorax without clotting.

If 1500 mL of blood is immediately drained or if the rate of ongoing blood loss exceeds 200 mL per hour for 2-4 hours, early thoracotomy should be considered.

Klumpke’s palsy, also known as Dejerine-Klumpke palsy, is a condition where the arm becomes paralyzed due to an injury to the lower roots of the brachial plexus. The most commonly affected root is C8, but T1 can also be involved. The main cause of Klumpke’s palsy is when the arm is pulled forcefully in an outward position during a difficult childbirth. It can also occur in adults with apical lung carcinoma (Pancoast’s syndrome).

Clinically, Klumpke’s palsy is characterized by a deformity known as ‘claw hand’, which is caused by the paralysis of the intrinsic hand muscles. There is also a loss of sensation along the ulnar side of the forearm and hand. In some cases where T1 is affected, a condition called Horner’s syndrome may also be present.

Klumpke’s palsy can be distinguished from Erb’s palsy, which affects the upper roots of the brachial plexus (C5 and sometimes C6). In Erb’s palsy, the arm hangs by the side with the elbow extended and the forearm turned inward (known as the ‘waiter’s tip sign’). Additionally, there is a loss of shoulder abduction, external rotation, and elbow flexion.

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

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

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

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

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

Type I hypersensitivity reactions are allergic reactions that occur when a person is exposed again to a particular antigen, known as an allergen. These reactions are triggered by IgE and typically happen within 15 to 30 minutes after exposure to the allergen.

A rapid onset of an urticarial rash, which occurs shortly after being exposed to an allergen (such as latex), is highly likely to be caused by a type I hypersensitivity reaction.

The risk of contracting meningococcal disease from a close contact is low. However, the risk is highest within the first seven days after the disease is diagnosed and decreases significantly afterwards.

Prophylaxis or vaccination for close contacts is typically organized by secondary care. It is recommended for the following individuals, regardless of their meningococcal vaccination status:

– People who have had prolonged close contact with the infected person in a household-type setting during the seven days prior to the onset of illness. This includes individuals living or sleeping in the same household, students in the same dormitory, partners, or university students sharing a kitchen in a hall of residence.

– People who have had brief close contact with the infected person, but only if they have been directly exposed to large particle droplets or secretions from the respiratory tract of the case around the time of admission to the hospital.

Antibiotic prophylaxis should be administered as soon as possible, ideally within 24 hours after the diagnosis of the index case.

Post-exposure prophylaxis is recommended for healthcare staff who have been exposed to direct nasopharyngeal secretions (without wearing a mask or personal protective equipment) from a known or highly probable case. This includes situations such as mouth-to-mouth resuscitation, airway management (suction/intubation), or prolonged close care within 1 meter of the patient who has been coughing or sneezing droplet secretions.

For more information, you can refer to the NICE Clinical Knowledge Summary on the management of close contacts of patients with meningococcal disease.

The complete blood count findings indicate a severe case of iron deficiency anemia. The patient’s red blood cells are significantly reduced in number, and there is a noticeable hypochromic microcytic anemia. When examining the peripheral blood smear, variations in shape (poikilocytosis) and size (anisocytosis) can be observed, which are typical of iron deficiency anemia. Pencil cells are commonly seen in this condition. Additionally, it is common for iron deficiency anemia to be accompanied by thrombocytosis, an increase in platelet count.

Heat stroke is a condition characterized by a core temperature higher than 40.6°C, accompanied by changes in mental state and varying levels of organ dysfunction. There are two forms of heat stroke: classic non-exertional heat stroke, which occurs during high environmental temperatures and typically affects elderly patients during heat waves, and exertional heat stroke, which occurs during strenuous physical exercise in hot conditions, such as endurance athletes competing in hot weather.

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

In the management of heat stroke, benzodiazepines like diazepam can be helpful in patients with agitation and/or shivering. They help reduce excessive heat production and agitation. In severe cases, patients may require paralysis. Antipyretics like paracetamol, aspirin, and NSAIDs have no role in the treatment of heat stroke. They do not work because the hypothalamus, which regulates body temperature, is healthy but overloaded in heat stroke. Moreover, antipyretics may actually be harmful in patients who develop complications like liver, blood, and kidney problems as they can worsen bleeding tendencies.

Dantrolene is commonly used in the treatment of heat stroke, although there is currently no high-level evidence to support its use. Neuroleptics, such as chlorpromazine, which were once commonly used, should be avoided due to their potential adverse effects, including lowering the seizure threshold, interfering with thermoregulation, causing anticholinergic side effects, hypotension, and hepatotoxicity.

The OPG is the recommended first-line imaging test for diagnosing TMJ dislocation and mandibular fractures.

Further Reading:

Mandibular fractures are a common type of facial fracture that often present to the emergency department. The mandible, or lower jaw, is formed by the fusion of two hemimandibles and articulates with the temporomandibular joints. Fractures of the mandible are typically caused by direct lateral force and often involve multiple fracture sites, including the body, condylar head and neck, and ramus.

When assessing for mandibular fractures, clinicians should use a look, feel, move method similar to musculoskeletal examination. However, it is important to note that TMJ effusion, muscle spasm, and pain can make moving the mandible difficult. Key signs of mandibular fracture include malocclusion, trismus (limited mouth opening), pain with the mouth closed, broken teeth, step deformity, hematoma in the sublingual space, lacerations to the gum mucosa, and bleeding from the ear.

The Manchester Mandibular Fracture Decision Rule uses the absence of five exam findings (malocclusion, trismus, broken teeth, pain with closed mouth, and step deformity) to exclude mandibular fracture. This rule has been found to be 100% sensitive and 39% specific in detecting mandibular fractures. Imaging is an important tool in diagnosing mandibular fractures, with an OPG X-ray considered the best initial imaging for TMJ dislocation and mandibular fracture. CT may be used if the OPG is technically difficult or if a CT is being performed for other reasons, such as a head injury.

It is important to note that head injury often accompanies mandibular fractures, so a thorough head injury assessment should be performed. Additionally, about a quarter of patients with mandibular fractures will also have a fracture of at least one other facial bone.

All individuals diagnosed with stage 5 chronic kidney disease should be given the option to choose between haemodialysis or peritoneal dialysis. Peritoneal dialysis should be prioritized as the preferred treatment for the following groups of patients: those who still have some remaining kidney function, adult patients without major additional health conditions, and children who are two years old or younger.

Eclampsia is the most likely diagnosis in this case. It is characterized by the occurrence of one or more convulsions on top of pre-eclampsia. To control seizures in eclampsia, the recommended treatment is magnesium sulphate. The Collaborative Eclampsia Trial regimen should be followed for administering magnesium sulphate. Initially, a loading dose of 4 g should be given intravenously over 5 to 15 minutes. This should be followed by a continuous infusion of 1 g per hour for 24 hours. If the woman experiences another eclamptic seizure, the infusion should be continued for an additional 24 hours after the last seizure. In case of recurrent seizures, a further dose of 2-4 g should be administered intravenously over 5 to 15 minutes. It is important to note that the only cure for eclampsia is the delivery of the fetus and placenta. Once the patient is stabilized, she should be prepared for an emergency caesarean section.

To manage aortic dissection, it is important to lower the systolic blood pressure to a range of 100-120 mmHg. This helps decrease the strain on the damaged artery and minimizes the chances of the dissection spreading further. In this patient, symptoms such as tearing chest pain and a widened mediastinum on the chest X-ray are consistent with aortic dissection.

Further Reading:

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

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

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

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

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

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

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

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

Acne conglobata is an extremely severe form of acne where acne nodules come together and create sinuses. Acne fulminans, on the other hand, is a rare and severe complication of acne conglobata that is accompanied by systemic symptoms. It is linked to elevated levels of androgenic hormones, specific autoimmune conditions, and a genetic predisposition.

The typical clinical characteristics of acne fulminans are as follows:

– Sudden and abrupt onset
– Inflammatory and ulcerated nodular acne primarily found on the chest and back
– Often painful lesions
– Ulcers on the upper trunk covered with bleeding crusts
– Severe acne scarring
– Fluctuating fever
– Painful joints and arthropathy
– General feeling of illness (malaise)
– Loss of appetite and weight loss
– Enlarged liver and spleen (hepatosplenomegaly)

It is crucial to refer patients immediately for a specialist evaluation and hospital admission. Treatment options for acne fulminans include systemic corticosteroids, dapsone, ciclosporin, and high-dose intravenous antibiotics.

The following provides a summary of common causes for different acid-base disorders.

Respiratory alkalosis can be caused by hyperventilation, such as during periods of anxiety. It can also be a result of conditions like pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, or the early stages of aspirin overdose.

Respiratory acidosis, on the other hand, is often associated with chronic obstructive pulmonary disease (COPD), life-threatening asthma, pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or other respiratory conditions.

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

Metabolic acidosis with a raised anion gap can be caused by lactic acidosis (such as in cases of hypoxemia, shock, sepsis, or infarction), ketoacidosis (such as in diabetes, starvation, or alcohol excess), renal failure, or poisoning (such as in late stages of aspirin overdose, methanol or ethylene glycol ingestion).

Lastly, metabolic acidosis with a normal anion gap can be a result of conditions like diarrhea, ammonium chloride ingestion, or adrenal insufficiency.

Urinary alkalinisation, which involves the intravenous administration of sodium bicarbonate, carries the risk of hypokalaemia. It is important to note that both alkalosis and acidosis can cause shifts in potassium levels. In the case of alkalinisation, potassium is shifted from the plasma into the cells. Therefore, it is crucial to closely monitor the patient for hypokalaemia by checking their potassium levels every 1-2 hours.

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.

Sialolithiasis is a condition in which a calcified stone (sialolith) forms inside a salivary gland. The submandibular gland (Wharton’s duct) is the most common site, accounting for about 90% of cases, while the parotid gland is the second most affected. In rare instances, sialoliths can also develop in the sublingual gland or minor salivary glands.

The presence of a sialolith obstructs the flow of saliva, leading to pain and swelling in the affected gland during eating. The pain is most intense when salivary flow is high, such as before and during meals, and gradually subsides within an hour after eating. By palpating the floor of the mouth with both hands, a stone may be detected, and sometimes it can even be seen at the opening of the duct. If there is an accompanying infection, pus may be expressed from the gland.

To assess salivary flow, acidic foods like lemon juice can be used as a simple test. X-rays of the mouth’s floor can reveal the presence of a stone. Patients should be referred to an ear, nose, and throat specialist (ENT) for the removal of the stone.

Sialadenitis refers to inflammation of the salivary glands and can be either acute or chronic. Acute sialadenitis is most commonly caused by a bacterial infection, usually ascending from Staphylococcus aureus or Streptococcus viridans. It can occur as a result of sialolithiasis or poor oral hygiene. Clinically, there will be a painful swelling in the affected gland area, with redness of the overlying skin and potential swelling of the cheek and nearby regions. Patients often experience general malaise, with a low-grade fever and elevated inflammatory markers.

Parotitis, on the other hand, refers to inflammation of one or both parotid glands. This inflammation can be caused by bacteria (particularly Staphylococcus aureus), viruses (such as mumps), or tuberculosis.

Sjögren’s syndrome is an autoimmune disorder characterized by dry eyes and dry mouth.

When suxamethonium is administered for neuromuscular blockade during rapid sequence induction, one of the clinical observations typically seen is muscle fasciculations. However, when rocuronium is used instead, muscle fasciculations are not present.

Further Reading:

Rapid sequence induction (RSI) is a method used to place an endotracheal tube (ETT) in the trachea while minimizing the risk of aspiration. It involves inducing loss of consciousness while applying cricoid pressure, followed by intubation without face mask ventilation. The steps of RSI can be remembered using the 7 P’s: preparation, pre-oxygenation, pre-treatment, paralysis and induction, protection and positioning, placement with proof, and post-intubation management.

Preparation involves preparing the patient, equipment, team, and anticipating any difficulties that may arise during the procedure. Pre-oxygenation is important to ensure the patient has an adequate oxygen reserve and prolongs the time before desaturation. This is typically done by breathing 100% oxygen for 3 minutes. Pre-treatment involves administering drugs to counter expected side effects of the procedure and anesthesia agents used.

Paralysis and induction involve administering a rapid-acting induction agent followed by a neuromuscular blocking agent. Commonly used induction agents include propofol, ketamine, thiopentone, and etomidate. The neuromuscular blocking agents can be depolarizing (such as suxamethonium) or non-depolarizing (such as rocuronium). Depolarizing agents bind to acetylcholine receptors and generate an action potential, while non-depolarizing agents act as competitive antagonists.

Protection and positioning involve applying cricoid pressure to prevent regurgitation of gastric contents and positioning the patient’s neck appropriately. Tube placement is confirmed by visualizing the tube passing between the vocal cords, auscultation of the chest and stomach, end-tidal CO2 measurement, and visualizing misting of the tube. Post-intubation management includes standard care such as monitoring ECG, SpO2, NIBP, capnography, and maintaining sedation and neuromuscular blockade.

Overall, RSI is a technique used to quickly and safely secure the airway in patients who may be at risk of aspiration. It involves a series of steps to ensure proper preparation, oxygenation, drug administration, and tube placement. Monitoring and post-intubation care are also important aspects of RSI.

Anaemia can be categorized based on the size of red blood cells. Microcytic anaemia, characterized by a mean corpuscular volume (MCV) of less than 80 fl, can be caused by various factors such as iron deficiency, thalassaemia, anaemia of chronic disease (which can also be normocytic), sideroblastic anaemia (which can also be normocytic), lead poisoning, and aluminium toxicity (although this is now rare and mainly affects haemodialysis patients).

On the other hand, normocytic anaemia, with an MCV ranging from 80 to 100 fl, can be attributed to conditions like haemolysis, acute haemorrhage, bone marrow failure, anaemia of chronic disease (which can also be microcytic), mixed iron and folate deficiency, pregnancy, chronic renal failure, and sickle-cell disease.

Lastly, macrocytic anaemia, characterized by an MCV greater than 100 fl, can be caused by factors such as B12 deficiency, folate deficiency, hypothyroidism, reticulocytosis, liver disease, alcohol abuse, myeloproliferative disease, myelodysplastic disease, and certain drugs like methotrexate, hydroxyurea, and azathioprine.

It is important to understand the different causes of anaemia based on red cell size as this knowledge can aid in the diagnosis and management of this condition.

Typically, children with viral gastroenteritis experience diarrhoea for a duration of 5-7 days. Vomiting, on the other hand, usually subsides within 1-2 days.

Further Reading:

Gastroenteritis is a common condition in children, particularly those under the age of 5. It is characterized by the sudden onset of diarrhea, with or without vomiting. The most common cause of gastroenteritis in infants and young children is rotavirus, although other viruses, bacteria, and parasites can also be responsible. Prior to the introduction of the rotavirus vaccine in 2013, rotavirus was the leading cause of gastroenteritis in children under 5 in the UK. However, the vaccine has led to a significant decrease in cases, with a drop of over 70% in subsequent years.

Norovirus is the most common cause of gastroenteritis in adults, but it also accounts for a significant number of cases in children. In England & Wales, there are approximately 8,000 cases of norovirus each year, with 15-20% of these cases occurring in children under 9.

When assessing a child with gastroenteritis, it is important to consider whether there may be another more serious underlying cause for their symptoms. Dehydration assessment is also crucial, as some children may require intravenous fluids. The NICE traffic light system can be used to identify the risk of serious illness in children under 5.

In terms of investigations, stool microbiological testing may be indicated in certain cases, such as when the patient has been abroad, if diarrhea lasts for more than 7 days, or if there is uncertainty over the diagnosis. U&Es may be necessary if intravenous fluid therapy is required or if there are symptoms and/or signs suggestive of hypernatremia. Blood cultures may be indicated if sepsis is suspected or if antibiotic therapy is planned.

Fluid management is a key aspect of treating children with gastroenteritis. In children without clinical dehydration, normal oral fluid intake should be encouraged, and oral rehydration solution (ORS) supplements may be considered. For children with dehydration, ORS solution is the preferred method of rehydration, unless intravenous fluid therapy is necessary. Intravenous fluids may be required for children with shock or those who are unable to tolerate ORS solution.

Antibiotics are generally not required for gastroenteritis in children, as most cases are viral or self-limiting. However, there are some exceptions, such as suspected or confirmed sepsis, Extraintestinal spread of bacterial infection, or specific infections like Clostridium difficile-associated pseudomembranous enterocolitis or giardiasis.

Alzheimer’s disease is characterized by various clinical features. These include memory loss, mood swings, apathy, and the presence of depressive or paranoid symptoms. Additionally, individuals with Alzheimer’s may experience Parkinsonism, a condition that affects movement, as well as a syndrome associated with the parietal lobe. Other symptoms may include difficulties with tasks such as copying 2D drawings, dressing properly, and carrying out a sequence of actions. Furthermore, individuals may struggle with copying gestures and may exhibit denial of their disorder, known as anosognosia. Topographical agnosia, or getting lost in familiar surroundings, may also be present, along with sensory inattention and astereognosis, which is the inability to identify objects when placed in the hand. Ultimately, Alzheimer’s disease is characterized by a relentless progression of personality and intellectual deterioration.

Based on the given information, the most likely diagnosis for the 4-year-old female patient is viral gastroenteritis. This is supported by the symptoms of vomiting and diarrhea, as well as the fact that the patient has been drinking less than usual and has vomited after being given a drink. The absence of recent travel and up-to-date immunizations also suggest that this is a viral rather than a bacterial infection.

Further Reading:

Gastroenteritis is a common condition in children, particularly those under the age of 5. It is characterized by the sudden onset of diarrhea, with or without vomiting. The most common cause of gastroenteritis in infants and young children is rotavirus, although other viruses, bacteria, and parasites can also be responsible. Prior to the introduction of the rotavirus vaccine in 2013, rotavirus was the leading cause of gastroenteritis in children under 5 in the UK. However, the vaccine has led to a significant decrease in cases, with a drop of over 70% in subsequent years.

Norovirus is the most common cause of gastroenteritis in adults, but it also accounts for a significant number of cases in children. In England & Wales, there are approximately 8,000 cases of norovirus each year, with 15-20% of these cases occurring in children under 9.

When assessing a child with gastroenteritis, it is important to consider whether there may be another more serious underlying cause for their symptoms. Dehydration assessment is also crucial, as some children may require intravenous fluids. The NICE traffic light system can be used to identify the risk of serious illness in children under 5.

In terms of investigations, stool microbiological testing may be indicated in certain cases, such as when the patient has been abroad, if diarrhea lasts for more than 7 days, or if there is uncertainty over the diagnosis. U&Es may be necessary if intravenous fluid therapy is required or if there are symptoms and/or signs suggestive of hypernatremia. Blood cultures may be indicated if sepsis is suspected or if antibiotic therapy is planned.

Fluid management is a key aspect of treating children with gastroenteritis. In children without clinical dehydration, normal oral fluid intake should be encouraged, and oral rehydration solution (ORS) supplements may be considered. For children with dehydration, ORS solution is the preferred method of rehydration, unless intravenous fluid therapy is necessary. Intravenous fluids may be required for children with shock or those who are unable to tolerate ORS solution.

Antibiotics are generally not required for gastroenteritis in children, as most cases are viral or self-limiting. However, there are some exceptions, such as suspected or confirmed sepsis, Extraintestinal spread of bacterial infection, or specific infections like Clostridium difficile-associated pseudomembranous enterocolitis or giardiasis.

Lidocaine functions by inhibiting the activity of voltage-gated sodium channels, preventing the flow of sodium ions through these channels.

Further Reading:

In the management of respiratory and cardiac arrest, several drugs are commonly used to help restore normal function and improve outcomes. Adrenaline is a non-selective agonist of adrenergic receptors and is administered intravenously at a dose of 1 mg every 3-5 minutes. It works by causing vasoconstriction, increasing systemic vascular resistance (SVR), and improving cardiac output by increasing the force of heart contraction. Adrenaline also has bronchodilatory effects.

Amiodarone is another drug used in cardiac arrest situations. It blocks voltage-gated potassium channels, which prolongs repolarization and reduces myocardial excitability. The initial dose of amiodarone is 300 mg intravenously after 3 shocks, followed by a dose of 150 mg after 5 shocks.

Lidocaine is an alternative to amiodarone in cardiac arrest situations. It works by blocking sodium channels and decreasing heart rate. The recommended dose is 1 mg/kg by slow intravenous injection, with a repeat half of the initial dose after 5 minutes. The maximum total dose of lidocaine is 3 mg/kg.

Magnesium sulfate is used to reverse myocardial hyperexcitability associated with hypomagnesemia. It is administered intravenously at a dose of 2 g over 10-15 minutes. An additional dose may be given if necessary, but the maximum total dose should not exceed 3 g.

Atropine is an antagonist of muscarinic acetylcholine receptors and is used to counteract the slowing of heart rate caused by the parasympathetic nervous system. It is administered intravenously at a dose of 500 mcg every 3-5 minutes, with a maximum dose of 3 mg.

Naloxone is a competitive antagonist for opioid receptors and is used in cases of respiratory arrest caused by opioid overdose. It has a short duration of action, so careful monitoring is necessary. The initial dose of naloxone is 400 micrograms, followed by 800 mcg after 1 minute. The dose can be gradually escalated up to 2 mg per dose if there is no response to the preceding dose.

It is important for healthcare professionals to have knowledge of the pharmacology and dosing schedules of these drugs in order to effectively manage respiratory and cardiac arrest situations.

Women have three options when requesting emergency contraception. The first option is Levonelle 1.5 mg, which contains levonorgestrel and can be used up to 72 hours after unprotected sexual intercourse (UPSI). If vomiting occurs within 2 hours of taking the tablet, another one should be given. Levonelle mainly works by preventing ovulation.

The second option is ulipristal acetate, the newest treatment available. It can be used up to 120 hours after UPSI. If vomiting occurs within 3 hours of ingestion, another tablet should be given. Ulipristal acetate also works by inhibiting ovulation. However, it should be avoided in patients taking enzyme-inducing drugs, those with severe hepatic impairment, or those with severe asthma requiring oral steroids.

The third option is the copper IUD, which can be fitted up to 5 days after UPSI or ovulation, whichever is longer. The failure rate of the copper IUD is less than 1 in 1000, making it 10-20 times more effective than oral emergency contraceptive options. It is important to note that Levonelle and ulipristal may be less effective in women with higher BMIs.

The GCS scoring system evaluates a patient’s level of consciousness based on three criteria: eye opening, verbal response, and motor response. Each criterion is assigned a score, and the total score determines the patient’s GCS score. For example, if a patient has a GCS score of 10 (E3 V2 M5), it means they scored 3 out of 4 in eye opening, 2 out of 5 in verbal response, and 5 out of 6 in motor response.

Further Reading:

A subdural hematoma (SDH) is a condition where there is a collection of blood between the dura mater and the arachnoid mater of the brain. It occurs when the cortical bridging veins tear and bleed into the subdural space. Risk factors for SDH include head trauma, cerebral atrophy, advancing age, alcohol misuse, and certain medications or bleeding disorders. SDH can be classified as acute, subacute, or chronic depending on its age or speed of onset. Acute SDH is typically the result of head trauma and can progress to become chronic if left untreated.

The clinical presentation of SDH can vary depending on the nature of the condition. In acute SDH, patients may initially feel well after a head injury but develop more serious neurological symptoms later on. Chronic SDH may be detected after a CT scan is ordered to investigate confusion or cognitive decline. Symptoms of SDH can include increasing confusion, progressive decline in neurological function, seizures, headache, loss of consciousness, and even death.

Management of SDH involves an ABCDE approach, seizure management, confirming the diagnosis with CT or MRI, checking clotting and correcting coagulation abnormalities, managing raised intracranial pressure, and seeking neurosurgical opinion. Some SDHs may be managed conservatively if they are small, chronic, the patient is not a good surgical candidate, and there are no neurological symptoms. Neurosurgical intervention typically involves a burr hole craniotomy to decompress the hematoma. In severe cases with high intracranial pressure and significant brain swelling, a craniectomy may be performed, where a larger section of the skull is removed and replaced in a separate cranioplasty procedure.

CT imaging can help differentiate between subdural hematoma and other conditions like extradural hematoma. SDH appears as a crescent-shaped lesion on CT scans.