When starting treatment with strong opioids for pain relief in palliative care, it is recommended to offer patients regular oral sustained-release or oral immediate-release morphine, depending on their preference. In addition, provide rescue doses of oral immediate-release morphine for breakthrough pain. For patients without renal or hepatic comorbidities, a typical total daily starting dose schedule of 20-30 mg of oral morphine is suggested, along with 5 mg of oral immediate-release morphine for rescue doses during the titration phase. It is important to adjust the dose until a good balance is achieved between pain control and side effects. If this balance is not reached after a few dose adjustments, it is advisable to seek specialist advice. Patients should be reviewed frequently, especially during the titration phase. For patients with moderate to severe renal or hepatic impairment, it is recommended to consult a specialist before prescribing strong opioids.

For maintenance therapy, oral sustained-release morphine is recommended as the first-line treatment for patients with advanced and progressive disease who require strong opioids. Transdermal patch formulations should not be routinely offered as first-line maintenance treatment unless oral opioids are not suitable. If pain remains inadequately controlled despite optimizing first-line maintenance treatment, it is important to review the analgesic strategy and consider seeking specialist advice.

When it comes to breakthrough pain, oral immediate-release morphine should be offered as the first-line rescue medication for patients on maintenance oral morphine treatment. Fast-acting fentanyl should not be offered as the first-line rescue medication. If pain continues to be inadequately controlled despite optimizing treatment, it may be necessary to seek specialist advice.

In cases where oral opioids are not suitable and analgesic requirements are stable, transdermal patches with the lowest acquisition cost can be considered. However, it is important to consult a specialist for guidance if needed. Similarly, for patients in whom oral opioids are not suitable and analgesic requirements are unstable, subcutaneous opioids with the lowest acquisition cost can be considered, with specialist advice if necessary.

For more information, please refer to the NICE Clinical Knowledge Summary: Opioids for pain relief in palliative care. https://www.nice.org.uk/guidance/cg140

Diabetic amyotrophy, also referred to as proximal diabetic neuropathy, is the second most prevalent form of diabetic neuropathy. It typically begins with discomfort in the buttocks, hips, or thighs and is often initially experienced on one side. The pain may start off as mild and gradually progress or it can suddenly manifest, as seen in this case. Subsequently, weakness and wasting of the proximal muscles in the lower limbs occur, making it difficult for the patient to transition from sitting to standing without assistance. Reflexes in the affected areas can also be impacted. Good control of blood sugar levels, physiotherapy, and lifestyle adjustments can reverse diabetic amyotrophy.

Peripheral neuropathy is the most common type of diabetic neuropathy and typically manifests as pain or loss of sensation in the feet or hands.

Autonomic neuropathy leads to changes in digestion, bowel and bladder function, sexual response, and perspiration. It can also affect the cardiovascular system, resulting in rapid heart rates and orthostatic hypotension.

Focal neuropathy causes sudden weakness in a single nerve or group of nerves, resulting in pain, sensory loss, or muscle weakness. Any nerve in the body can be affected.

The BTS guidelines for acute asthma in children recommend administering oral steroids early in the treatment of asthma attacks. It is advised to give a dose of 20 mg prednisolone for children aged 2–5 years and a dose of 30–40 mg for children over 5 years old. If a child is already taking maintenance steroid tablets, they should receive 2 mg/kg prednisolone, up to a maximum dose of 60 mg. If a child vomits after taking the medication, the dose of prednisolone should be repeated. In cases where a child is unable to keep down orally ingested medication, intravenous steroids should be considered. Typically, treatment for up to three days is sufficient, but the duration of the course should be adjusted based on the time needed for recovery. Tapering off the medication is not necessary unless the steroid course exceeds 14 days. For more information, refer to the BTS/SIGN Guideline on the Management of Asthma.

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

Further Reading:

A pneumothorax is an abnormal collection of air in the pleural cavity of the lung. It can be classified by cause as primary spontaneous, secondary spontaneous, or traumatic. Primary spontaneous pneumothorax occurs without any obvious cause in the absence of underlying lung disease, while secondary spontaneous pneumothorax occurs in patients with significant underlying lung diseases. Traumatic pneumothorax is caused by trauma to the lung, often from blunt or penetrating chest wall injuries.

Tension pneumothorax is a life-threatening condition where the collection of air in the pleural cavity expands and compresses normal lung tissue and mediastinal structures. It can be caused by any of the aforementioned types of pneumothorax. Immediate management of tension pneumothorax involves the ABCDE approach, which includes ensuring a patent airway, controlling the C-spine, providing supplemental oxygen, establishing IV access for fluid resuscitation, and assessing and managing other injuries.

Treatment of tension pneumothorax involves needle thoracocentesis as a temporary measure to provide immediate decompression, followed by tube thoracostomy as definitive management. Needle thoracocentesis involves inserting a 14g cannula into the pleural space, typically via the 4th or 5th intercostal space midaxillary line. If the patient is peri-arrest, immediate thoracostomy is advised.

The pathophysiology of tension pneumothorax involves disruption to the visceral or parietal pleura, allowing air to flow into the pleural space. This can occur through an injury to the lung parenchyma and visceral pleura, or through an entry wound to the external chest wall in the case of a sucking pneumothorax. Injured tissue forms a one-way valve, allowing air to enter the pleural space with inhalation but prohibiting air outflow. This leads to a progressive increase in the volume of non-absorbable intrapleural air with each inspiration, causing pleural volume and pressure to rise within the affected hemithorax.

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

In this scenario, there are similarities between hypothyroidism and perimenopause in terms of their features. However, the most frequent cause of experiencing these symptoms together is depression. Therefore, it is necessary to delve deeper into this woman’s mood to rule out depression and provide appropriate management.

To exclude hypothyroidism as a potential cause, a TSH blood test should be conducted. Additionally, it is important to inquire about other symptoms that may align with early menopause.

Lithium is a commonly prescribed medication for bipolar disorder, as it helps stabilize mood. The recommended therapeutic range for lithium levels is typically between 0.4 and 0.8 mmol/l, although this range may vary depending on the laboratory. For maintenance therapy and treatment in older individuals, the lower end of the range is usually targeted. Toxic effects of lithium are typically observed when levels exceed 1.5 mmol/l. It is important to monitor lithium levels one week after starting therapy and after any dosage adjustments.

One potential side effect of lithium is the development of nephrogenic diabetes insipidus, a condition that affects the kidneys’ ability to concentrate urine. However, lithium does not cause diabetes mellitus. Another known side effect is hypothyroidism, which is a decrease in thyroid hormone production, but it does not lead to hyperthyroidism, an overactive thyroid.

Signs of lithium toxicity include nausea, vomiting, diarrhea, tremors, ataxia (loss of coordination), confusion, increased muscle tone, clonus (repetitive, involuntary muscle contractions), nephrogenic diabetes insipidus, convulsions, coma, and renal failure. It is crucial to be aware of these symptoms and seek medical attention if they occur.

The most significant factor in predicting postoperative nausea and vomiting (PONV) is being female. Females are three times more likely than males to experience PONV. Additionally, not smoking increases the risk of PONV by about two times. Having a history of motion sickness, PONV, or both also approximately doubles the risk of PONV. Age is another factor, with older adults being less likely to suffer from PONV. In children, those below 3 years of age have a lower risk of PONV compared to those older than 3.

Further Reading:

postoperative nausea and vomiting (PONV) is a common occurrence following procedures performed under sedation or anesthesia. It can be highly distressing for patients. Several risk factors have been identified for PONV, including female gender, a history of PONV or motion sickness, non-smoking status, patient age, use of volatile anesthetics, longer duration of anesthesia, perioperative opioid use, use of nitrous oxide, and certain types of surgery such as abdominal and gynecological procedures.

To manage PONV, antiemetics are commonly used. These medications work by targeting different receptors in the body. Cyclizine and promethazine are histamine H1-receptor antagonists, which block the action of histamine and help reduce nausea and vomiting. Ondansetron is a serotonin 5-HT3 receptor antagonist, which blocks the action of serotonin and is effective in preventing and treating PONV. Prochlorperazine is a dopamine D2 receptor antagonist, which blocks the action of dopamine and helps alleviate symptoms of nausea and vomiting. Metoclopramide is also a dopamine D2 receptor antagonist and a 5-HT3 receptor antagonist, providing dual action against PONV. It is also a 5-HT4 receptor agonist, which helps improve gastric emptying and reduces the risk of PONV.

Assessment and management of PONV involves a comprehensive approach. Healthcare professionals need to assess the patient’s risk factors for PONV and take appropriate measures to prevent its occurrence. This may include selecting the appropriate anesthesia technique, using antiemetics prophylactically, and providing adequate pain control. In cases where PONV does occur, prompt treatment with antiemetics should be initiated to alleviate symptoms and provide relief to the patient. Close monitoring of the patient’s condition and response to treatment is essential to ensure effective management of PONV.

Hepatic encephalopathy is a condition caused by the accumulation of nitrogenous waste products in the body due to impaired liver function. These waste products cross the blood brain barrier and contribute to the production of glutamine, leading to changes in astrocyte osmotic pressure, brain edema, and neurotransmitter dysfunction.

To address hepatic encephalopathy, the first-line drugs used are Rifaximin and lactulose. Rifaximin is an oral antibiotic that helps reduce the presence of ammonia-producing bacteria in the intestines. Lactulose, on the other hand, converts soluble ammonia into insoluble ammonium and aids in relieving constipation.

It is important to note that Chlordiazepoxide, a benzodiazepine, may be used to treat alcohol withdrawal but should be avoided in cases of hepatic encephalopathy as it can worsen the condition.

Further Reading:

Cirrhosis is a condition where the liver undergoes structural changes, resulting in dysfunction of its normal functions. It can be classified as either compensated or decompensated. Compensated cirrhosis refers to a stage where the liver can still function effectively with minimal symptoms, while decompensated cirrhosis is when the liver damage is severe and clinical complications are present.

Cirrhosis develops over a period of several years due to repeated insults to the liver. Risk factors for cirrhosis include alcohol misuse, hepatitis B and C infection, obesity, type 2 diabetes, autoimmune liver disease, genetic conditions, certain medications, and other rare conditions.

The prognosis of cirrhosis can be assessed using the Child-Pugh score, which predicts mortality based on parameters such as bilirubin levels, albumin levels, INR, ascites, and encephalopathy. The score ranges from A to C, with higher scores indicating a poorer prognosis.

Complications of cirrhosis include portal hypertension, ascites, hepatic encephalopathy, variceal hemorrhage, increased infection risk, hepatocellular carcinoma, and cardiovascular complications.

Diagnosis of cirrhosis is typically done through liver function tests, blood tests, viral hepatitis screening, and imaging techniques such as transient elastography or acoustic radiation force impulse imaging. Liver biopsy may also be performed in some cases.

Management of cirrhosis involves treating the underlying cause, controlling risk factors, and monitoring for complications. Complications such as ascites, spontaneous bacterial peritonitis, oesophageal varices, and hepatic encephalopathy require specific management strategies.

Overall, cirrhosis is a progressive condition that requires ongoing monitoring and management to prevent further complications and improve outcomes for patients.

Bell’s palsy is a condition characterized by sudden weakness or paralysis of the facial nerve, resulting in facial muscle weakness or drooping. The exact cause is unknown, but it is believed to be related to viral infections such as herpes simplex or varicella zoster. It is more common in individuals aged 15-45 years and those with diabetes, obesity, hypertension, or upper respiratory conditions. Pregnancy is also a risk factor.

Diagnosis of Bell’s palsy is typically based on clinical symptoms and ruling out other possible causes of facial weakness. Symptoms include rapid onset of unilateral facial muscle weakness, drooping of the eyebrow and corner of the mouth, loss of the nasolabial fold, otalgia, difficulty chewing or dry mouth, taste disturbance, eye symptoms such as inability to close the eye completely, dry eye, eye pain, and excessive tearing, numbness or tingling of the cheek and mouth, speech articulation problems, and hyperacusis.

When assessing a patient with facial weakness, it is important to consider other possible differentials such as stroke, facial nerve tumors, Lyme disease, granulomatous diseases, Ramsay Hunt syndrome, mastoiditis, and chronic otitis media. Red flags for these conditions include insidious and painful onset, duration of symptoms longer than 3 months with frequent relapses, pre-existing risk factors, systemic illness or fever, vestibular or hearing abnormalities, and other cranial nerve involvement.

Management of Bell’s palsy involves the use of steroids, eye care advice, and reassurance. Steroids, such as prednisolone, are recommended for individuals presenting within 72 hours of symptom onset. Eye care includes the use of lubricating eye drops, eye ointment at night, eye taping if unable to close the eye at night, wearing sunglasses, and avoiding dusty environments. Reassurance is important as the majority of patients make a complete recovery within 3-4 months. However, some individuals may experience sequelae such as facial asymmetry, gustatory lacrimation, inadequate lid closure, brow ptosis, drooling, and hemifacial spasms.

Antiviral treatments are not currently recommended as a standalone treatment for Bell’s palsy, but they may be given in combination with corticosteroids on specialist advice. Referral to an ophthalmologist is necessary if the patient has eye symptoms such as pain, irritation, or itch.

Cauda equina syndrome (CES) is a rare but serious complication that can occur when a disc ruptures. This happens when the material from the disc is pushed into the spinal canal and puts pressure on the bundle of nerves in the lower back and sacrum. As a result, individuals may experience loss of control over their bladder and bowel functions.

There are certain red flags that may indicate the presence of CES. These include experiencing sciatica on both sides of the body, having severe or worsening neurological issues in both legs (such as significant weakness in knee extension, ankle eversion, or foot dorsiflexion), difficulty starting urination or a decreased sensation of urinary flow, loss of sensation in the rectum, experiencing numbness or tingling in the perianal, perineal, or genital areas (also known as saddle anesthesia or paresthesia), and having a lax anal sphincter.

Conus medullaris syndrome (CMS) is a condition that affects the conus medullaris, which is located above the cauda equina at the T12-L2 level. Unlike CES, CMS primarily causes back pain and may have less noticeable nerve root pain. The main symptoms of CMS are urinary retention and constipation.

To confirm a diagnosis of CES and determine the level of compression and any underlying causes, an MRI scan is considered the gold-standard investigation. In cases where an MRI is not possible or contraindicated, a CT myelogram or standard CT scans can be helpful. However, plain radiographs have limited value and may only show significant degenerative or traumatic bone diseases.

Addison’s disease occurs when the adrenal glands do not produce enough steroid hormones. This includes glucocorticoids, mineralocorticoids, and sex steroids. The most common cause is autoimmune adrenalitis, which accounts for about 70-80% of cases. It is more prevalent in women and typically occurs between the ages of 30 and 50.

The clinical symptoms of Addison’s disease include weakness, lethargy, low blood pressure (especially when standing up), nausea, vomiting, weight loss, reduced hair in the armpits and pubic area, depression, and hyperpigmentation (darkening of the skin in certain areas like the palms, mouth, and exposed skin).

Biochemically, Addison’s disease is characterized by increased levels of ACTH (a hormone that tries to stimulate the adrenal glands), low sodium levels, high potassium levels, high calcium levels, low blood sugar, and metabolic acidosis.

People with Addison’s disease have a higher risk of developing type 1 diabetes, Hashimoto’s thyroiditis, Grave’s disease, premature ovarian failure, pernicious anemia, vitiligo, and alopecia.

Management of Addison’s disease should be overseen by an Endocrinologist. Treatment typically involves taking hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also need thyroxine if there is hypothalamic-pituitary disease present. Treatment is lifelong, and patients should carry a steroid card and a MedicAlert bracelet in case of an Addisonian crisis.

ACE inhibitors should not be used in individuals with HAE because they can enhance the effects of bradykinin. This can lead to drug-induced angioedema, which is a known side effect of ACE inhibitors. In individuals with HAE, ACE inhibitors can trigger attacks of angioedema.

Further Reading:

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

Activated charcoal is a commonly utilized substance for decontamination in cases of poisoning. Its main function is to attract and bind molecules of the ingested toxin onto its surface.

Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. This powder is created by subjecting carbonaceous matter to high heat, a process known as pyrolysis, and then concentrating it with a solution of zinc chloride. Through this process, the activated charcoal develops a complex network of pores, providing it with a large surface area of approximately 3,000 m2/g. This extensive surface area allows it to effectively hinder the absorption of the harmful toxin by up to 50%.

The typical dosage for adults is 50 grams, while children are usually given 1 gram per kilogram of body weight. Activated charcoal can be administered orally or through a nasogastric tube. It is crucial to administer it within one hour of ingestion, and if necessary, a second dose may be repeated after one hour.

Theophylline, a medication commonly used to treat respiratory conditions, can be affected by certain drugs, either increasing or decreasing its plasma concentration and half-life. Drugs that can increase the plasma concentration of theophylline include calcium channel blockers like verapamil, cimetidine, fluconazole, macrolides such as erythromycin, methotrexate, and quinolones like ciprofloxacin. On the other hand, drugs like carbamazepine, phenobarbitol, phenytoin (and fosphenytoin), rifampicin, and St. John’s wort can decrease the plasma concentration of theophylline. It is important to be aware of these interactions when prescribing or taking theophylline to ensure its effectiveness and avoid potential side effects.

A varicocele is a condition characterized by the presence of varicose veins in the pampiniform plexus of the cord and scrotum. It is more commonly observed in the left testis compared to the right and may be linked to infertility. The primary reason for this association is believed to be the elevated temperature of the testis caused by the presence of varicosities.

Typically, individuals with varicocele experience a dull ache in the testis, which tends to worsen after physical activity or towards the end of the day. The scrotum is often described as feeling like a bag of worms. While the varicocele cannot usually be detected when the patient is lying down, it can often be identified during examination while standing. It is felt as a poorly defined, non-transilluminable mass that is clearly separate from the testis and is located above and behind it. The dilation of the varicocele increases when the Valsalva maneuver is performed, and a cough impulse may also be present.

Conservative treatment is typically recommended for varicocele, with surgery being reserved for severe cases only.

This individual is diagnosed with an acquired cholesteatoma, which is an expanding growth of the stratified keratinising epithelium in the middle ear. It develops due to dysfunction of the Eustachian tube and chronic otitis media caused by the retraction of the squamous elements of the tympanic membrane into the middle ear space.

The most important method for assessing the presence of a cholesteatoma is otoscopy. A retraction pocket observed in the attic or posterosuperior quadrant of the tympanic membrane is a characteristic sign of an acquired cholesteatoma. This is often accompanied by the presence of granulation tissue and squamous debris. The presence of a granular polyp within the ear canal also strongly suggests a cholesteatoma.

If left untreated, a cholesteatoma can lead to various complications including conductive deafness, facial nerve palsy, brain abscess, meningitis, and labyrinthitis. Therefore, it is crucial to urgently refer this individual to an ear, nose, and throat (ENT) specialist for a CT scan and surgical removal of the lesion.

Narrow QRS complex tachycardia is a term used to describe a fast heart rhythm with a pulse rate over 100 bpm and a QRS duration shorter than 120 ms.

Further Reading:

Supraventricular tachycardia (SVT) is a type of tachyarrhythmia that originates from the atria or above the bundle of His in the heart. It includes all atrial and junctional tachycardias, although atrial fibrillation is often considered separately. SVT typically produces a narrow QRS complex tachycardia on an electrocardiogram (ECG), unless there is an underlying conduction abnormality below the atrioventricular (AV) node. Narrow complex tachycardias are considered SVTs, while some broad complex tachycardias can also be SVTs with co-existent conduction delays.

SVT can be classified into three main subtypes based on where it arises: re-entrant accessory circuits (the most common type), atrial tachycardias, and junctional tachycardias. The most common SVTs are AVNRT (AV nodal re-entry tachycardia) and AVRT (AV re-entry tachycardia), which arise from accessory circuits within the heart. AVNRT involves an accessory circuit within the AV node itself, while AVRT involves an accessory pathway between the atria and ventricles that allows additional electrical signals to trigger the AV node.

Atrial tachycardias originate from abnormal foci within the atria, except for the SA node, AV node, or accessory pathway. Junctional tachycardias arise in the AV junction. The ECG features of SVTs vary depending on the type. Atrial tachycardias may have abnormal P wave morphology, an isoelectric baseline between P waves (in atrial flutter), and inverted P waves in certain leads. AVNRT may show pseudo R waves in V1 or pseudo S waves in certain leads, with an RP interval shorter than the PR interval. AVRT (WPW) may exhibit a delta wave on a resting ECG and retrograde P waves in the ST segment, with an RP interval shorter than the PR interval. Junctional tachycardias may have retrograde P waves before, during, or after the QRS complex, with inverted P waves in certain leads and upright P waves in others.

Treatment of SVT follows the 2021 resuscitation council algorithm for tachycardia with a pulse. The algorithm provides guidelines for managing stable patients with SVT.

Inserting an IJV line on the right side of the neck is preferred because it reduces the risk of damaging the thoracic duct. The thoracic duct is where the largest lymphatic vessel in the body connects to the bloodstream. It is situated where the left subclavian and internal jugular veins meet, as well as the beginning of the brachiocephalic vein. Opting for the right side of the neck helps prevent potential harm to the thoracic duct.

Further Reading:

A central venous catheter (CVC) is a type of catheter that is inserted into a large vein in the body, typically in the neck, chest, or groin. It has several important uses, including CVP monitoring, pulmonary artery pressure monitoring, repeated blood sampling, IV access for large volumes of fluids or drugs, TPN administration, dialysis, pacing, and other procedures such as placement of IVC filters or venous stents.

When inserting a central line, it is ideal to use ultrasound guidance to ensure accurate placement. However, there are certain contraindications to central line insertion, including infection or injury to the planned access site, coagulopathy, thrombosis or stenosis of the intended vein, a combative patient, or raised intracranial pressure for jugular venous lines.

The most common approaches for central line insertion are the internal jugular, subclavian, femoral, and PICC (peripherally inserted central catheter) veins. The internal jugular vein is often chosen due to its proximity to the carotid artery, but variations in anatomy can occur. Ultrasound can be used to identify the vessels and guide catheter placement, with the IJV typically lying superficial and lateral to the carotid artery. Compression and Valsalva maneuvers can help distinguish between arterial and venous structures, and doppler color flow can highlight the direction of flow.

In terms of choosing a side for central line insertion, the right side is usually preferred to avoid the risk of injury to the thoracic duct and potential chylothorax. However, the left side can also be used depending on the clinical situation.

Femoral central lines are another option for central venous access, with the catheter being inserted into the femoral vein in the groin. Local anesthesia is typically used to establish a field block, with lidocaine being the most commonly used agent. Lidocaine works by blocking sodium channels and preventing the propagation of action potentials.

In summary, central venous catheters have various important uses and should ideally be inserted using ultrasound guidance. There are contraindications to their insertion, and different approaches can be used depending on the clinical situation. Local anesthesia is commonly used for central line insertion, with lidocaine being the preferred agent.

Shingles is caused by the varicella-zoster virus (VZV), which primarily infects individuals during childhood as chickenpox. However, the initial infection can also be subclinical. After the primary infection, the virus remains dormant in the sensory nervous system, specifically in the geniculate, trigeminal, or dorsal root ganglia.

During the dormant phase, the virus is kept under control by the immune system for many years. However, it can later become active and cause a flare-up in a specific dermatomal segment. This reactivation occurs when the virus travels down the affected nerve over a period of 3 to 5 days, leading to inflammation within and around the nerve. The decline in cell-mediated immunity is believed to trigger the virus’s reactivation.

Several factors can trigger the reactivation of the varicella-zoster virus, including advancing age (with most patients being older than 50), immunosuppressive illnesses, physical trauma, and psychological stress. In immunocompetent patients, the most common site of reactivation is the thoracic nerves, followed by the ophthalmic division of the trigeminal nerve.

Diagnosing shingles can usually be done based on the patient’s history and clinical examination alone, as it has a distinct history and appearance. While various techniques can be used to detect the virus or antibodies, they are often unnecessary. Microscopy and culture tests using scrapings and smears typically yield negative results.