The current guidelines from NICE and the BNF suggest that if treatment is necessary for campylobacter enteritis, clarithromycin should be the first choice. Azithromycin and erythromycin can be used interchangeably, and ciprofloxacin is a suitable alternative. It is important to note that many cases of campylobacter enteritis resolve on their own without treatment. However, individuals with severe infections or those who are immunocompromised should receive treatment.

When a patient is semi-conscious, it is less likely for the nasopharyngeal airway adjuncts (NPA’s) to trigger the gag reflex compared to oropharyngeal airways. Therefore, NPA’s are typically the preferred option in these cases.

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.

Shenton’s line is a useful tool for identifying hip fractures on radiographs. It is a curved line that is drawn along the bottom edge of the upper pubic bone and the inner lower edge of the femur neck. This line should be smooth and uninterrupted. If there are any breaks or irregularities in the line, it could indicate a fracture, dysplasia, or dislocation.

Further Reading:

Fractured neck of femur is a common injury, especially in elderly patients who have experienced a low impact fall. Risk factors for this type of fracture include falls, osteoporosis, and other bone disorders such as metastatic cancers, hyperparathyroidism, and osteomalacia.

There are different classification systems for hip fractures, but the most important differentiation is between intracapsular and extracapsular fractures. The blood supply to the femoral neck and head is primarily from ascending cervical branches that arise from an arterial anastomosis between the medial and lateral circumflex branches of the femoral arteries. Fractures in the intracapsular region can damage the blood supply and lead to avascular necrosis (AVN), with the risk increasing with displacement. The Garden classification can be used to classify intracapsular neck of femur fractures and determine the risk of AVN. Those at highest risk will typically require hip replacement or arthroplasty.

Fractures below or distal to the capsule are termed extracapsular and can be further described as intertrochanteric or subtrochanteric depending on their location. The blood supply to the femoral neck and head is usually maintained with these fractures, making them amenable to surgery that preserves the femoral head and neck, such as dynamic hip screw fixation.

Diagnosing hip fractures can be done through radiographs, with Shenton’s line and assessing the trabecular pattern of the proximal femur being helpful techniques. X-rays should be obtained in both the AP and lateral views, and if an occult fracture is suspected, an MRI or CT scan may be necessary.

In terms of standards of care, it is important to assess the patient’s pain score within 15 minutes of arrival in the emergency department and provide appropriate analgesia within the recommended timeframes. Patients with moderate or severe pain should have their pain reassessed within 30 minutes of receiving analgesia. X-rays should be obtained within 120 minutes of arrival, and patients should be admitted within 4 hours of arrival.

NICE provides the following recommendations for the treatment of non-pregnant women with lower urinary tract infections (UTIs):

1. Consider prescribing a back-up antibiotic or an immediate antibiotic for women with lower UTIs, taking into account the severity of symptoms, the risk of complications, previous urine culture results, previous antibiotic use, and the woman’s preferences.

2. If a urine sample has been sent for culture and susceptibility testing and an antibiotic prescription has been given, review the choice of antibiotic when the microbiological results are available. Change the antibiotic according to susceptibility results if bacteria are resistant and symptoms are not improving.

3. The first-choice antibiotics for non-pregnant women aged 16 years and over are nitrofurantoin (100 mg modified-release tablets taken twice daily for 3 days) or trimethoprim (200 mg tablets taken twice daily for 3 days), if there is a low risk of resistance.

4. If there is no improvement in lower UTI symptoms after at least 48 hours on the first-choice antibiotic or if the first-choice antibiotic is not suitable, the second-choice options are nitrofurantoin (100 mg modified-release tablets taken twice daily for 3 days), pivmecillinam (400 mg initial dose followed by 200 mg three times daily for 3 days), or fosfomycin (3 g single sachet dose).

5. The risk of resistance to antibiotics may be lower if the antibiotic has not been used in the past 3 months, previous urine culture suggests susceptibility, and in younger people in areas with low resistance rates. The risk of resistance may be higher with recent antibiotic use and in older people in residential facilities.

This explanation suggests that the patient’s symptoms are consistent with a case of travellers diarrhoea, which is in line with their medical history. GBS typically occurs within 1-3 weeks after the initial viral or bacterial infection that caused it.

Further Reading:

Campylobacter jejuni is a common cause of gastrointestinal infections, particularly travellers diarrhoea. It is a gram-negative bacterium that appears as curved rods. The infection is transmitted through the feco-oral route, often through the ingestion of contaminated meat, especially poultry. The incubation period for Campylobacter jejuni is typically 1-7 days, and the illness usually lasts for about a week.

The main symptoms of Campylobacter jejuni infection include watery, and sometimes bloody, diarrhea accompanied by abdominal cramps, fever, malaise, and headache. In some cases, complications can arise from the infection. Guillain-Barre syndrome (GBS) is one such complication that is associated with Campylobacter jejuni. Approximately 30% of GBS cases are caused by this bacterium.

When managing Campylobacter jejuni infection, conservative measures are usually sufficient, with a focus on maintaining hydration. However, in cases where symptoms are severe, such as high fever, bloody diarrhea, or high-output diarrhea, or if the person is immunocompromised, antibiotics may be necessary. NICE recommends the use of clarithromycin, administered at a dose of 250-500 mg twice daily for 5-7 days, starting within 3 days of the onset of illness.

Digoxin toxicity can be triggered by hypokalaemia, a condition characterized by low levels of potassium in the body. This occurs because digoxin competes with potassium for binding sites, and when potassium levels are low, there is less competition for digoxin to bind to these sites. Additionally, other factors such as hypomagnesaemia, hypercalcaemia, hypernatraemia, and acidosis can also contribute to digoxin toxicity.

Further Reading:

Digoxin is a medication used for rate control in atrial fibrillation and for improving symptoms in heart failure. It works by decreasing conduction through the atrioventricular node and increasing the force of cardiac muscle contraction. However, digoxin toxicity can occur, and plasma concentration alone does not determine if a patient has developed toxicity. Symptoms of digoxin toxicity include feeling generally unwell, lethargy, nausea and vomiting, anorexia, confusion, yellow-green vision, arrhythmias, and gynaecomastia.

ECG changes seen in digoxin toxicity include downsloping ST depression with a characteristic Salvador Dali sagging appearance, flattened, inverted, or biphasic T waves, shortened QT interval, mild PR interval prolongation, and prominent U waves. There are several precipitating factors for digoxin toxicity, including hypokalaemia, increasing age, renal failure, myocardial ischaemia, electrolyte imbalances, hypoalbuminaemia, hypothermia, hypothyroidism, and certain medications such as amiodarone, quinidine, verapamil, and diltiazem.

Management of digoxin toxicity involves the use of digoxin specific antibody fragments, also known as Digibind or digifab. Arrhythmias should be treated, and electrolyte disturbances should be corrected with close monitoring of potassium levels. It is important to note that digoxin toxicity can be precipitated by hypokalaemia, and toxicity can then lead to hyperkalaemia.

Pelvic inflammatory disease (PID) is a pelvic infection that affects the upper female reproductive tract, including the uterus, fallopian tubes, and ovaries. It is typically caused by an ascending infection from the cervix and is commonly associated with sexually transmitted diseases like chlamydia and gonorrhea. In the UK, genital Chlamydia trachomatis infection is the most common cause of PID seen in genitourinary medicine clinics.

PID can often be asymptomatic, but when symptoms are present, they may include lower abdominal pain and tenderness, fever, painful urination, painful intercourse, purulent vaginal discharge, abnormal vaginal bleeding, and tenderness in the cervix and adnexa. It is important to note that symptoms of ectopic pregnancy can be similar to those of PID, so a pregnancy test should be conducted for all patients with suspicious symptoms.

To investigate a possible case of PID, endocervical swabs should be taken to test for C. trachomatis and N. gonorrhoeae using nucleic acid amplification tests if available. Mild to moderate cases of PID can usually be managed in primary care or outpatient settings, while patients with severe disease should be admitted to the hospital for intravenous antibiotics. Signs of severe disease include a fever above 38°C, signs of a tubo-ovarian abscess, signs of pelvic peritonitis, or concurrent pregnancy.

Empirical antibiotic treatment should be initiated as soon as a presumptive diagnosis of PID is made clinically, without waiting for swab results. The current recommended outpatient treatment for PID is a single intramuscular dose of ceftriaxone 500 mg, followed by oral doxycycline 100 mg twice daily and oral metronidazole 400 mg twice daily for 14 days. An alternative regimen is oral ofloxacin 400 mg twice daily and oral metronidazole 400 mg twice daily for 14 days.

For severely ill patients in the inpatient setting, initial treatment includes intravenous doxycycline, a single-dose of intravenous ceftriaxone, and intravenous metronidazole. This is then followed by a switch to oral doxycycline and metronidazole to complete a 14-day treatment course. If a patient fails to respond to treatment, laparoscopy is necessary to confirm the diagnosis or consider alternative diagnoses.

Conn’s syndrome, also known as primary hyperaldosteronism, is often characterized by hypertension along with hypokalaemia and hypernatraemia. On the other hand, Addison’s disease typically leads to hypotension, hyponatremia, and hyperkalaemia. Hyponatraemia is commonly associated with pituitary adenoma, while acute renal failure (ARF) is characterized by elevated levels of urea and creatinine, and hyperkalaemia is frequently observed in ARF.

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.

Anterior uveitis refers to the inflammation of the iris and is characterized by a painful and red eye. It is often accompanied by symptoms such as sensitivity to light, excessive tearing, and a decrease in visual clarity. In less than 10% of cases, the inflammation may extend to the posterior chamber. The condition can also lead to the formation of adhesions between the iris and the lens or cornea, resulting in an irregularly shaped pupil known as synechia. In severe cases, pus may accumulate in the front part of the eye, specifically the anterior chamber, causing a condition called hypopyon.

There are various factors that can cause anterior uveitis, including idiopathic cases where no specific cause can be identified. Other causes include trauma, chronic joint diseases like spondyloarthropathies and juvenile chronic arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriasis, sarcoidosis, and infections such as Lyme disease, tuberculosis, leptospirosis, herpes simplex virus (HSV), and varicella-zoster virus (VZV). It is worth noting that approximately 50% of patients with anterior uveitis have a strong association with the HLA-B27 genotype.

Complications that can arise from uveitis include the development of cataracts, glaucoma, band keratopathy (a condition where calcium deposits form on the cornea), and even blindness.

Erb’s palsy, also known as Erb-Duchenne palsy, is a condition where the arm becomes paralyzed due to an injury to the upper roots of the brachial plexus. The primary root affected is usually C5, although C6 may also be involved in some cases. The main cause of Erb’s palsy is when the arm experiences excessive force during a difficult childbirth, but it can also occur in adults as a result of shoulder trauma.

Clinically, the affected arm will hang by the side with the elbow extended and the forearm turned inward (known as the waiter’s tip sign). Upon examination, there will be a loss of certain movements:

– Shoulder abduction (involving the deltoid and supraspinatus muscles)
– Shoulder external rotation (infraspinatus muscle)
– Elbow flexion (biceps and brachialis muscles)

It is important to differentiate Erb’s palsy from Klumpke’s palsy, which affects the lower roots of the brachial plexus (C8 and T1). Klumpke’s palsy presents with a claw hand due to paralysis of the intrinsic hand muscles, along with sensory loss along the ulnar side of the forearm and hand. If T1 is affected, there may also be the presence of Horner’s syndrome.