Peripheral and central vertigo can be differentiated based on certain characteristics. Peripheral vertigo typically has a sudden onset and is associated with more severe symptoms of vertigo. The vertigo symptoms may come and go intermittently. Individuals with peripheral vertigo often experience severe nausea and vomiting. Their vertigo is also affected by head movement, particularly in certain positions. Peripheral vertigo is usually not accompanied by any focal neurology. Nystagmus, which is an involuntary eye movement, tends to occur away from the side of the lesion. In some cases, hearing may also be impaired, as seen in conditions like Meniere’s disease and labyrinthitis.

On the other hand, central vertigo tends to have a gradual onset and milder symptoms of vertigo. The vertigo symptoms are constant and do not fluctuate. Nausea and vomiting may be present but are usually less severe compared to peripheral vertigo. Unlike peripheral vertigo, central vertigo is not influenced by head movement and is considered fixed. Individuals with central vertigo may experience new-onset headaches. Additionally, central vertigo is often accompanied by focal neurology, indicating involvement of specific areas of the brain. Nystagmus in central vertigo occurs towards the side of the lesion. Unlike peripheral vertigo, hearing is typically unaffected in central vertigo cases.

This patient is likely to have pigeon fancier’s lung, which is a type of extrinsic allergic alveolitis (EAA) caused by chronic exposure to avian antigens found in bird droppings. This condition leads to hypersensitivity pneumonitis and the formation of granulomas in the lungs.

While his presentation could also be consistent with idiopathic pulmonary fibrosis, the fact that he keeps and races pigeons makes EAA more likely in this case.

EAA can manifest as either an acute or chronic condition. The acute form typically presents with flu-like symptoms such as fever, cough, chest tightness, and breathlessness occurring 4 to 6 hours after exposure.

The clinical features of chronic pigeon fancier’s lung include a productive cough, progressive breathlessness, weight loss, anorexia, fatigue, and malaise.

Other forms of EAA include farmer’s lung (caused by exposure to Saccharopolyspora rectivirgula from wet hay), malt-worker’s lung (caused by exposure to Aspergillus clavatus from moldy malt), cheese-worker’s lung (caused by exposure to Penicillium casei from moldy cheese), chemical worker’s lung (caused by exposure to trimetallic anhydride, diisocyanate, and methylene diisocyanate), mushroom worker’s lung (caused by exposure to thermophilic actinomycetes in mushroom compost), and hot tub lung (caused by exposure to Mycobacterium avium from poorly maintained hot tubs).

Spontaneous bacterial peritonitis (SBP) is a sudden bacterial infection of the fluid in the abdomen. It typically occurs in patients with high blood pressure in the portal vein, and about 70% of patients are classified as Child-Pugh class C. In any given year, around 30% of patients with ascites, a condition characterized by fluid buildup in the abdomen, will develop SBP.

SBP can present with a wide range of symptoms, so it’s important to be vigilant when caring for patients with ascites, especially if there is a sudden decline in their condition. Some patients may not show any symptoms at all.

Common clinical features of SBP include fever, chills, nausea, vomiting, abdominal pain, tenderness, worsening ascites, general malaise, and hepatic encephalopathy. Certain factors can increase the risk of developing SBP, such as severe liver disease, gastrointestinal bleeding, urinary tract infection, intestinal bacterial overgrowth, indwelling lines (e.g., central venous catheters or urinary catheters), previous episodes of SBP, and low levels of protein in the ascitic fluid.

To diagnose SBP, an abdominal paracentesis, also known as an ascitic tap, is performed. This involves locating the area of dullness on the flank, next to the rectus abdominis muscle, and performing the tap about 5 cm above and towards the midline from the anterior superior iliac spines.

Certain features on the analysis of the peritoneal fluid strongly suggest SBP, including a total white cell count in the ascitic fluid of more than 500 cells/µL, a total neutrophil count of more than 250 cells/µL, a lactate level in the ascitic fluid of more than 25 mg/dL, a pH of less than 7.35, and the presence of bacteria on Gram-stain.

Patients diagnosed with SBP should be admitted to the hospital and given broad-spectrum antibiotics. The preferred choice is an intravenous 3rd generation cephalosporin, such as ceftriaxone. If the patient is allergic to beta-lactam antibiotics, ciprofloxacin can be considered as an alternative. Administering intravenous albumin can help reduce the risk of kidney failure and mortality.

Wernicke’s encephalopathy is a condition that is commonly associated with alcohol abuse and other causes of thiamine deficiency. It is characterized by a classic triad of symptoms, which include acute confusion, ophthalmoplegia (paralysis or weakness of the eye muscles), and ataxia (loss of coordination and balance). Additional possible features of this condition may include papilloedema (swelling of the optic disc), hearing loss, apathy, dysphagia (difficulty swallowing), memory impairment, and hypothermia. In the majority of cases, peripheral neuropathy (nerve damage) is also observed, typically affecting the legs.

The condition is marked by the presence of acute capillary haemorrhages, astrocytosis (abnormal increase in astrocytes, a type of brain cell), and neuronal death in the upper brainstem and diencephalon. These abnormalities can be visualized using MRI scanning, while CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will go on to develop a Korsakoff psychosis. This condition is characterized by retrograde amnesia (difficulty remembering past events), an inability to memorize new information, disordered time appreciation, and confabulation (fabrication of false memories).

Hypertension, hyperglycemia, weight gain, truncal obesity, supraclavicular fat pads, and striae are characteristic symptoms of a Cushing syndrome.

Further Reading:

Cushing’s syndrome is a clinical syndrome caused by prolonged exposure to high levels of glucocorticoids. The severity of symptoms can vary depending on the level of steroid exposure. There are two main classifications of Cushing’s syndrome: ACTH-dependent disease and non-ACTH-dependent disease. ACTH-dependent disease is caused by excessive ACTH production from the pituitary gland or ACTH-secreting tumors, which stimulate excessive cortisol production. Non-ACTH-dependent disease is characterized by excess glucocorticoid production independent of ACTH stimulation.

The most common cause of Cushing’s syndrome is exogenous steroid use. Pituitary adenoma is the second most common cause and the most common endogenous cause. Cushing’s disease refers specifically to Cushing’s syndrome caused by an ACTH-producing pituitary tumor.

Clinical features of Cushing’s syndrome include truncal obesity, supraclavicular fat pads, buffalo hump, weight gain, moon facies, muscle wasting and weakness, diabetes or impaired glucose tolerance, gonadal dysfunction, hypertension, nephrolithiasis, skin changes (such as skin atrophy, striae, easy bruising, hirsutism, acne, and hyperpigmentation in ACTH-dependent causes), depression and emotional lability, osteopenia or osteoporosis, edema, irregular menstrual cycles or amenorrhea, polydipsia and polyuria, poor wound healing, and signs related to the underlying cause, such as headaches and visual problems.

Diagnostic tests for Cushing’s syndrome include 24-hour urinary free cortisol, 1 mg overnight dexamethasone suppression test, and late-night salivary cortisol. Other investigations aim to assess metabolic disturbances and identify the underlying cause, such as plasma ACTH, full blood count (raised white cell count), electrolytes, and arterial blood gas analysis. Imaging, such as CT or MRI of the abdomen, chest, and/or pituitary, may be required to assess suspected adrenal tumors, ectopic ACTH-secreting tumors, and pituitary tumors. The choice of imaging is guided by the ACTH result, with undetectable ACTH and elevated serum cortisol levels indicating ACTH-independent Cushing’s syndrome and raised ACTH suggesting an ACTH-secreting tumor.

In this case, the most appropriate target parameter to guide oxygen therapy would be an SpO2 (oxygen saturation) level of greater than 94%.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

This man is experiencing an acute asthma episode. His initial peak flow is 55% of his best, indicating a moderate exacerbation. In such cases, it is recommended to administer steroids, specifically a dose of prednisolone 40-50 mg orally.

Chest X-rays are not routinely performed to investigate acute asthma. However, they should be considered in certain situations, including suspected pneumomediastinum, consolidation, life-threatening asthma, inadequate response to treatment, and the need for ventilation.

Nebulised ipratropium bromide is only added to treatment with nebulised salbutamol in patients with acute severe or life-threatening asthma, or those who do not respond well to salbutamol therapy. Therefore, it is not necessary in this particular case.

While it may be reasonable to prescribe an antihistamine for a patient with a history of worsening hay fever, it should not be prioritized over treatment with steroids.

The typical range for the normal angle of Gissane is between 120 and 145 degrees. An increase in this angle suggests that the posterior facet of the subtalar joint is depressed, which may indicate a calcaneal fracture. Similarly, the normal range for Bohler’s angle is between 20 and 40 degrees. For more detailed information and visual representations of these angles, please refer to the accompanying notes.

Further Reading:

calcaneus fractures are a common type of lower limb and joint injury. The calcaneus, or heel bone, is the most frequently fractured tarsal bone. These fractures are often intra-articular, meaning they involve the joint. The most common cause of calcaneus fractures is a fall or jump from a height.

When assessing calcaneus fractures, X-rays are used to visualize the fracture lines. Two angles are commonly assessed to determine the severity of the fracture. Böhler’s angle, which measures the angle between two tangent lines drawn across the anterior and posterior borders of the calcaneus, should be between 20-40 degrees. If it is less than 20 degrees, it indicates a calcaneal fracture with flattening. The angle of Gissane, which measures the depression of the posterior facet of the subtalar joint, should be between 120-145 degrees. An increased angle of Gissane suggests a calcaneal fracture.

In the emergency department, the management of a fractured calcaneus involves identifying the injury and any associated injuries, providing pain relief, elevating the affected limb(s), and referring the patient to an orthopedic specialist. It is important to be aware that calcaneus fractures are often accompanied by other injuries, such as bilateral fractures of vertebral fractures.

The definitive management of a fractured calcaneus can be done conservatively or through surgery, specifically open reduction internal fixation (ORIF). The orthopedic team will typically order a CT or MRI scan to classify the fracture and determine the most appropriate treatment. However, a recent UK heel fracture trial suggests that in most cases, ORIF does not improve fracture outcomes.

The primary approach to managing nerve gas exposure through medication involves the repeated administration of antidotes. The two antidotes utilized for this purpose are atropine and pralidoxime.

Atropine is the standard anticholinergic medication employed to address the symptoms associated with nerve agent poisoning. It functions as an antagonist for muscarinic acetylcholine receptors, effectively blocking the effects caused by excessive acetylcholine. Initially, a 1.2 mg intravenous bolus of atropine is administered. This dosage is then repeated and doubled every 2-3 minutes until excessive bronchial secretion ceases and miosis (excessive constriction of the pupil) resolves. In some cases, as much as 100 mg of atropine may be necessary.

Pralidoxime (2-PAMCl) is the standard oxime used in the treatment of nerve agent poisoning. Its mechanism of action involves reactivating acetylcholinesterase by scavenging the phosphoryl group attached to the functional hydroxyl group of the enzyme, thereby counteracting the effects of the nerve agent itself. For patients who are moderately or severely poisoned, pralidoxime should be administered intravenously at a dosage of 30 mg/kg of body weight (or 2 g in the case of an adult) over a period of four minutes.

When assessing a patient with epistaxis (nosebleed), it is important to start with a standard ABC assessment, focusing on the airway and hemodynamic status. Even if the bleeding appears to have stopped, it is crucial to evaluate the patient’s airway and circulation.

If active bleeding is still present and there are signs of hemodynamic compromise, immediate resuscitative and first aid measures should be initiated. Epistaxis should be treated as a circulatory emergency, especially in elderly patients, those with clotting disorders or bleeding tendencies, and individuals taking anticoagulants. In these cases, it is necessary to establish intravenous access using at least an 18-gauge (green) cannula and collect blood samples for tests such as full blood count, urea and electrolytes, clotting studies, and blood typing and crossmatching (depending on the amount of blood loss). These patients should be closely monitored in a majors area or a designated observation area, as dislodgement of a blood clot can lead to severe bleeding.

First aid measures to control bleeding include the following steps:
1. The patient should be seated upright with their body tilted forward and their mouth open. Lying down should be avoided, unless the patient feels faint or there are signs of hemodynamic compromise. Leaning forward helps reduce the flow of blood into the back of the throat.
2. The patient should be encouraged to spit out any blood that enters the throat and advised not to swallow it.
3. Firmly pinch the soft, cartilaginous part of the nose, compressing the nostrils for 10-15 minutes. Pressure should not be released, and the patient should breathe through their mouth.
4. If the patient is unable to comply with pinching their own nose, an alternative technique is to ask a relative or staff member to apply external pressure using a device like a swimmer’s nose clip.
5. It is important to dispel the misconception that compressing the bones of the nose will help stop the bleeding. Applying ice to the neck or forehead has not been proven to affect nasal blood flow. However, sucking on an ice cube or applying an ice pack directly to the nose may help reduce nasal blood flow.

If bleeding stops with first aid measures, it may be beneficial to apply a topical antiseptic preparation to reduce crusting and inflammation. Naseptin cream (containing chlorhexidine and neomycin) is commonly used and should be applied to the nostrils four times daily for 10 days.