Spinal Stenosis Doctor Instruction: Your next patient is a 51-year-old woman called Rebecca, presenting with lower back pain. Please take a history and perform an appropriate examination. Patient History: Rebecca, a 51-year-old female, nurse You have always been having lower back pain for the past few years, but this has been getting gradually worse. The pain is dull and intermittent. Very often, the pain can diffuse and radiate towards the buttocks, back of the thighs, and feet - when this happens, the pain feels like a burning or cramping sensation. It can be associated with weakness in both legs. The symptoms can be triggered or worsened by sitting down, standing straight and walking downhill. It goes away after a few minutes after being at rest. Bending forward improves symptoms. You tried paracetamol, which only helped a little with pain. If you walk for more than 50 yards, you will start noticing numbness and weakness in your legs. No previous injury/trauma. Waterworks normal. The bowels are working normally. No other abnormal sensations or weaknesses. No incontinence. No stiffness. No fever. No weight loss. No night sweats. Ideas, Concerns, Expectations: You think because you often have to bend your back due to work, the pain may be caused by poor posture. You are concerned because it is starting to affect your ability to work in the hospital as a nurse. You would like to see if you can get stronger painkillers and possibly have a scan of your back. Past Medical History: Obesity, hypercholesterolemia, acromegaly, T2DM. No past relevant surgical history. Drug History: Atorvastatin, metformin NKDA. Family History: Father has ankylosing spondylitis. Social History: You work as a senior nurse in a local hospital. You smoke around ten cigarettes daily for over ten years but don't drink alcohol. Live with husband in a semi-detached house. Independent. Examination Findings: Lower spinal tenderness on palpation at L4-5 region. Complete motor and sensory neurological examinations are normal. Features of acromegaly e.g. enlarged hands, feet and facial features. Lower limb vascular examination is normal. No cervical tenderness or restricted movement. Gait normal. No cauda equina syndrome features. Peripheral pulses and ABPI normal. Differentials: Lumbar spinal stenosis - likely to be due to degenerative changes Osteoarthritis of the spine To rule out cauda equina syndrome Ankylosing spondylitis/spondylolisthesis Rule out peripheral arterial diseases Other causes of back pain: spinal tumour, disc herniation, trauma, fracture, and epidural abscess. Investigations: Imaging: XR Lumbar spine (may show degenerative changes/spondylolisthesis) MRI Spine. Alternatively, CT myelography/spine when MRI is not available or unsuitable. Consider ABPI / CT angiogram to exclude peripheral arterial disease where intermittent claudications are present. Special tests: Consider electromyographic (EMG) walking test - increased F latency values in lumbar spinal stenosis Consider electromyographic paraspinal mapping Management: Conservative: Exercise Weight loss if overweight Physiotherapy e.g. exercises that minimally stress the back, such as walking, swimming, or bicycling. Exercise may also strengthen the paraspinal muscles. NSAIDSs e.g. naproxen, celecoxib +/- PPI cover / antacids Paracetamol Medication for neuropathic pain e.g. amitriptyline, gabapentin, pregabalin. Consider oral steroids for acute exacerbation of painful symptoms. Activity modification e.g. limit heavy lifting/prolonged sitting/repetitive bending/twisting of the back. Consider deep heat therapy with massage to relieve spasms associated with back pain Surgical: Consider decompression surgery +/- fusion e.g. laminectomy ( removal of the lamina from affected vertebra) followed by physiotherapy Consider interspinous distraction procedure to reduce backward movement of the spine. Consider epidural injections with local anaesthetic and corticosteroids under specialist guidance for short/long-term pain relief. Viva Questions: Explain the pathophysiology of spinal stenosis. Spinal stenosis is the narrowing of the spinal canal, which holds the spinal cord and nerves. It's often due to age-related disc degeneration, arthritis, and thickened ligaments. This narrowing can compress the spinal cord and nerves, leading to pain, numbness, and weakness. Factors like herniated discs and inflammation worsen the compression. Treatment involves pain management, physical therapy, and sometimes surgery to relieve pressure on the nerves and spinal cord. At what level of the spine does spinal stenosis occur most commonly? Spinal stenosis most commonly occurs in the lumbar (lower back) region of the spine. This is because the lumbar spine bears the most weight and undergoes significant movement, which can contribute to degenerative changes over time. Lumbar spinal stenosis can result in compression of the spinal cord and nerve roots, leading to symptoms such as lower back pain, leg pain, numbness, and weakness. However, spinal stenosis can also occur in the cervical (neck) and thoracic (mid-back) regions of the spine, albeit less frequently. What are the causes of spinal stenosis? Degeneration of spinal structures due to aging. Disc degeneration and herniation. Osteoarthritis and bone spurs. Thickened ligaments. Congenital factors and genetics. Injuries and trauma. Tumors or abnormal growths. These factors narrow the spinal canal, compressing nerves and causing stenosis symptoms. What are the risk factors of spinal stenosis? Age: Risk increases with aging. Genetics: Family history matters. Congenital: Narrow canal from birth. Injuries: Past spine trauma or surgery. Lifestyle: Heavy lifting, certain jobs. Obesity: Excess weight strains spine. Diseases: Arthritis, diabetes, etc. Scoliosis: Abnormal spine curvature. What are the red flag symptoms/signs of back pain? Neurological Issues: Weakness, numbness, or tingling. Bladder/Bowel Problems: Loss of control. Severe Pain: Unbearable or unrelenting. Fever: Along with back pain. Unexplained Weight Loss: Rapid and unintended. Cancer History: Especially if pain is new. Night Pain: Worse at night. Trauma: After injury or accident. Age Over 50: New-onset pain. Steroid Use: Especially long-term.

Cauda Equina Syndrome Doctor Instruction: You are currently a senior surgical doctor on call. Your next patient is a 45-year-old gentleman, Adam, who presents back pain after being hit by a slow-moving car yesterday. Please take a history and perform an appropriate examination. Patient History: Adam, a 45-year-old gentleman, banker You came in today following a small car collision towards your back while walking across the road last night. You brushed this off – thinking it was no big idea. However, you started noticing lower back pain with weakness in your lower limbs. Back pain is located centrally in the lower back – can sometimes radiate down both legs. You describe the pain as sharp, rating it 10/10. You tried many things to ease the pain without success e.g. paracetamol and ibuprofen. Back pain can be triggered by simple back movement but not worsened by coughing or straining. You have numbness and tingling sensation running down both of your legs. Also, while wiping yourself afterwards in the toilet, you couldn’t feel the sensation around your bottom as well as your genitals– it was very strange, and at that point, you knew you needed to go and seek medical attention. You developed incontinence for passing urine and faeces. You no longer have the urge to go the toilet, and they can come out involuntarily, which is very concerning for you—no other previous back injuries. Idea, Concern, Expectation: You have no idea what is going on, but you think it is related to yesterday's injury. You are very concerned and don’t want to be paralysed – you are still very young! You would like to find out what is going on. You are very scared if you need any surgery for this. Past Medical History: Hypertension, obesity Drug History: Ramipril, Atorvastatin NKDA Family History: Ankylosing Spondylitis Social History: Smoke 10 cigarettes/day for over 20 years Drink around 2-3 pints of beer every weekend Work as a banker Live with a wife and two kids in a semi-detached house Examination Findings: Both lower limbs power 4/5 with reduced sensations, tone, and reflexes. Lower back spinal tenderness at L3/4 region. PR Examination: Reduced anal tone and sensation. No upper motor neurone signs Differentials: Caudal Equina Syndrome caused by trauma Prolapsed lumbar disc Conus medullaris syndrome Mechanical back pain Peripheral neuropathy Spinal tumour Investigations: Basic observations Routine bloods for baseline and pre-assessment e.g. FBC, U&Es, LFT, Bone Profile, CRP Consider blood culture if suspected infection. Emergency MRI to confirm and exclude cauda equina syndrome Consider CT myelography/spine Consider XR spine Consider Urodynamic studies -to monitor bladder function Management (Cauda Equina Syndrome): Hospital Admission VTE prophylaxis Prevention of further damage e.g. Immobilise spine if CES is due to trauma Neurosurgical input for consideration of lumbar decompression surgery – the earlier this is performed, the higher the chance of regaining functions. Surgery may involve removing bone fragments, tumour, herniated disc, blood, debulking for SOL e.g. tumour abscess…etc. Anti-inflammatories such as steroids, if due to inflammatory cause For infectious causes, patients should be treated with antibiotics Postoperative care includes physiotherapy, occupational therapy, and addressing lifestyle issues e.g. obesity. Treatment for metastatic spinal cord compression includes analgesia, high-dose dexamethasone, surgery, radiotherapy, and chemotherapy. Investigations include biopsy, staging CT, PET scan…etc. Viva Questions: Explain the pathophysiology of cauda equina syndrome. Cauda equina syndrome is caused by compression of nerve roots at the base of the spine. This pressure leads to severe back pain, leg pain, numbness, weakness, and bladder/bowel dysfunction. Why is cauda equina syndrome a surgical emergency? Cauda equina syndrome is a surgical emergency because the compression of nerve roots can cause permanent and severe neurological damage. Prompt surgery is essential to prevent irreversible loss of sensation, muscle function, and bladder/bowel control. The urgency is to minimize lasting deficits and improve patient outcomes. Where does the spinal cord terminate (at what level)? The spinal cord typically terminates around the level of the first or second lumbar vertebra (L1-L2) in most adults. Below this point, the spinal cord transitions into a bundle of nerve roots known as the cauda equina, which continues down the vertebral canal and provides innervation to the lower extremities and pelvic organs What is conus medullaris? The conus medullaris is the tapering, lower end of the spinal cord. It is located at the termination of the spinal cord, usually around the level of the first or second lumbar vertebra (L1-L2). Below the conus medullaris, the spinal cord transitions into the cauda equina, a bundle of nerve roots that extend further down the spinal canal. The conus medullaris is an important anatomical landmark and holds significance in medical imaging, surgical procedures, and discussions related to spinal cord and neurological health. What are the causes of cauda equina syndrome? Cauda equina syndrome is caused by conditions that compress or damage the nerve roots at the base of the spinal cord. Common causes include herniated discs, spinal tumors, spinal stenosis, trauma, infections, inflammatory conditions, and postoperative complications. Immediate medical attention is crucial to prevent permanent nerve damage. Does cauda equina syndrome show lower or upper motor neurone signs or both? Cauda equina syndrome leads to signs and symptoms characteristic of lower motor neuron involvement. These include bilateral reduction in sensation of the lower limbs, impaired bladder and bowel function, weakness in the lower limb muscles, intense back pain, and potential issues with sexual function.

Gastro-Oesophageal Reflux Disease Doctor Instruction: You are a Foundation Year 1 Doctor working in the Emergency Department. Your next patient is a 42-year-old woman (Anne) presenting with abdominal pain. Please take a history and perform an appropriate examination. Patient History: Anne, a 42-year-old retired hairdresser. This morning at around 3am, you woke up from having tummy pain. Described as a sharp/burning sensation that started at the bottom chest centrally and radiated up to the neck. It is intermittent and lasts for a few seconds. Pain score: 5/10. You are known to have angina, and so you took a GTN spray, but it didn't help. You feel a bit nauseous but no vomiting; you had some retching (and a bad taste in the back of the throat). Pain tends to be worsened or triggered when you try to go back to bed and lay flat. If asked specifically, you remember having quite a big family meal when your friend came to visit the night before. No weight loss. No tiredness. No erosion in teeth. No bad-smelling mouth. No lump in the throat. No bloating. No nocturnal cough. No hoarse voice. Bowels working normally with no bloody stool. No breathing difficulty. No dysphagia. No LOC. No dizziness. No palpitation. No obvious chest pain. Ideas, Concerns, Expectations: You are not sure what is going on. You are worried that you had a heart attack and may die because of this since it is quite close to the chest. You want to be seen by a cardiologist and have some medications to help prevent having this pain again. You want to live! Past Medical History: Hypertension Stable angina - well-controlled Obesity Chronic Lower Back Pain Drug History: Amlodipine, GTN spray PRN, Atovastatin, ibuprofen NKDA Family History: Type 2 DM (Dad, age 44) Colon Cancer (Dad, age 65) Social History: Smoker – 10 cigarettes/day for 20 + years Drink a small glass of gin and tonic every night Hairdresser Drink 2 cups of coffee a day. Examination Findings: The patient is alert + comfortable at rest, with no signs of breathing difficulties. No clinical signs of anaemia. Some mild discomfort palpating the epigastric region. Abdominal examination is otherwise normal. PR exam is normal - no melena or blood in the stool. Differentials: GORD Gastritis Peptic ulcer Hiatus Hernia Oesophagitis / Oesophageal spasm To rule out cardiovascular causes: Stable Angina / ACS / AAA Investigations: Bedside: Observations ECG – rule out cardiac cause Bloods: FBC, CRP, U&Es, LFTs, Bone Profile, Troponin (if suspecting cardiac cause) Imaging: CXR/AXR (?Hiatus hernia) Special Tests: Consider serology/ urea breath test/ stool antigen, rapid urease test (H-pylori testing - ensure not taken PPI 2 weeks prior to testing) Barium swallow - assess dynamics, assess motility disorder, assess for hiatus hernia Oesophageal pH monitoring / Manometry - Assess for motility & regurgitative Disorders Consider OGD (Savary-Miller grading/ Los Angeles Classification) - allows direct visualisation and biopsy for histology. Data Interpretation: Patient Details: Alexander Great Age: 42 Date of Request: 18/04/2023 ​ Value Reference Range ​ Hb 125 g/L 115 - 165 g/L ​ White Cell Count 7.5 x10^9/L 3.6 - 11.0 x10^9/L ​ Platelets 257 x10^9/L 140 - 400 x10^9/L ​ Haematocrit 0.47 x10^12/L 0.40 - 0.54 x10^12/L ​ MCV 94 fL 80 - 100 fL ​ Neutrophils 3.7 x10^9/L 1 - 7.5 x10^9/L ​ Monocytes 0.7 x10^9/L 0.2 - 0.8 x10^9/L ​ Lymphocytes 3 x10^9/L 1 - 4 x10^9/L ​ Basophils 0.03 x10^9/L 0.02 - 0.1 ​ Eosinophils 0.1 0.1 - 0.4 ​ ​ ​ ​ ​ H. Pylori Stool Antigen Test Negative ​ Interpretation of Blood Results: ree Interpretation of OGD Image: Management (GORD): Conservative: Lifestyle changes: stop smoking, weight loss, reduce alcohol intake, sleep more upright, small + regular meals, avoid eating big meals/ alcohol/ hot drinks before bed, avoid triggering diet e.g. spicy food, citrus, chocolate, caffeine, carbonated drinks, alcohol, manage stress level Review medications that can cause reflux, e.g. NSAID, steroids, bisphosphonates, nitrates, calcium channel blockers, alpha/beta agonists, theophylline, anticholinergics Antacids e.g. Gaviscon PPI e.g. omeprazole H2 antagonist e.g. Ranitidine Patient Education Safety netting for uncontrolled and red flag symptoms e.g. ACS Medical: Eradication therapy if tested positive for H. Pylori (PPI plus 2 antibiotics e.g. amoxicillin and clarithromycin) for 7 days. Surgical: Surgery for reflux e.g. fundoplication, magnetic sphincter augmentation. Viva questions: What are the complications of untreated acid reflux? Esophagitis: Inflammation and pain in the esophagus. Barrett's Esophagus: Increased risk of esophageal cancer. Strictures: Narrowing of the esophagus. Esophageal Ulcers: Painful sores in the esophagus. Respiratory Issues: Coughing, wheezing, and asthma exacerbation. Dental Problems: Tooth enamel erosion and oral health issues. Chronic Cough: Persistent cough unrelated to respiratory problems. Laryngitis/Voice Changes: Hoarseness and vocal cord inflammation. Asthma Aggravation: Worsening of asthma symptoms. Difficulty Swallowing: Dysphagia due to esophageal changes. Esophageal Cancer: Increased cancer risk over time. What are the complications of long-term management with omeprazole? Electrolyte disturbance e.g. magnesium Low bone mineral density - interference in gastric pH which can alter calcium absorption What is Barrett's Oesophagus? Barrett's esophagus develops due to chronic acid reflux (GERD). Acid irritates the esophagus, prompting the lining to transform into a type more resistant to acid, called columnar cells. This change is known as metaplasia, resulting in Barrett's epithelium. This condition increases the risk of esophageal cancer, making regular monitoring crucial. What are the red flag symptoms or signs for urgent OGD? Haematemesis or melena Dysphagia Unintentional weight loss Treatment-resistant Early satiety Recurrent vomitting

Skin Infection Doctor Instruction: You are the on-call surgical senior hour officer covering Vascular Surgery and Plastic Surgery. Your next patient is called Lui, who is a 56-year-old man coming in with left leg pain. Please take a history and perform an appropriate examination. Patient History: Lui, a 56-year-old male, retired. Since last week, you have been getting worsening lower left leg pain around the on-going ulcer located at the front of your left lower leg. This ulcer has been there for many years, and the area around it is getting redder and warmer to touch. The skin feels really tense and thickened and looks swollen compared to the other leg. You are unsure if you have a fever as you don’t own a thermometer at home, but you sometimes shiver with occasional night sweats. Your appetite has reduced. You do not feel well. You feel tired. No fluid-filled blisters. No bleeding or discharge. No recent trauma or injury. No insect bites. No recent surgeries or immobility. No nausea or vomiting. No itchiness. The joints are normal. No abnormal sensation. No weakness. Ideas, Concerns, Expectations: You have no idea what this might be, but you heard from your friend that this might be something called “?DVT”, which your friend had following a hip replacement in the hospital. You are concerned about this, so you would like to find out what is happening! Past Medical History: Diabetes, obesity, venous insufficiency, venous ulcer left lower leg, IBD Drug History: Metformin, atorvastatin, azathioprine NKDA Family History: Diabetes, HTN Social History: Drink 2-4 cans of beer a night. No recreational drug use. Non-smoker. Live alone in a Bungalow – you will often have district nurses around for wound care of your ulcer for the past few years. Retired. Examination Findings: Venous ulcer at anterior left lower leg with surrounding warm and tender erythematous skin. Poorly demarcated redness. No skin crepitus. No blisters or vesicles. Varicose veins can be seen in both lower legs. No necrotic / gangrenous tissues. No pitting oedema. No toe-web abnormalities. – e.g. fissures, scaling, maceration. No injury/trauma site. Neurovascular intact. CRT < 2seconds. Differentials: Cellulitis Erysipelas Rule out DVT Rule out pyoderma granulosum/ necrotising fasciitis Superficial thrombophlebitis Varicose eczema Investigations: Cellulitis can be diagnosed clinically. Consider wound, skin swab/blood culture/aspiration/biopsy if appropriate. Consider referral to be seen at the hospital and for bloods if the patient is systemically unwell: FBC, CRP, U&E, LFT, Bone Profile, culture and perform sepsis 6 Consider assessing diabetic control: BM, serum glucose, hba1c Consider XR, USS, or MRI for assessing the spread of infection, e.g. bone, gas in subcutaneous tissue, abscesses, or involving foreign bodies…etc., at the hospital. Management: Conservative: Rest, elevation of affected limb and analgesia, e.g. paracetamol/ NSAID / opioid. Hydration VTE prophylaxis/assessment Clean affected site: irrigation, debride devitalised tissues if appropriate. Emollient to moisturise skin Imaging/drawing to assess the progression of spread/resolution with follow-up. Assess tetanus risk and status if punctured wound or laceration Safety netting if non-improving or worsening symptoms/ signs 48 hours after the course of antibiotic Medical: Consider hospital admission for severe cellulitis, immunocompromise, significant comorbidity, social issues, systematic illness, non-responsive to oral treatment, further deterioration, necrotising fasciitis, and orbital cellulitis. Consider referral to dermatology, surgery, or other specialists if appropriate for urgent review or advice. Flucloxacillin (Oral/IV), alternative: erythromycin, clarithromycin, clindamycin, doxycycline, co-amoxiclav. If MRSA is suspected, consider adding one of vancomycin, teicoplanin or linezolid to standard treatment. Long-course antibiotics for patients with lymphoedema until signs of acute inflammation have resolved – may take 1-2 months. Course otherwise is generally for seven days and can be extended to 10-14 days to ensure complete resolution. Surgical: If presenting crepitus/ necrotic appearing skin, this requires urgent surgical intervention to exclude necrotising fasciitis. Crepitus also requires urgent debridement of tissue. If symptoms or signs of osteomyelitis, or septic arthritis, this requires urgent orthopaedic input. Prevention: Good diabetic control Good wound/ulcer management: regular use of absorbent but non-adhesive dressing, aspirate / deroof blisters using aseptic technique as per local protocol Weight control Treatment of athlete’s foot if present For chronic limb swelling: elevation, calf muscle exercises, compression stockings (only when acute cellulitis has resolved) Appropriate footwear, treat neuropathy in diabetes and avoid injury to the skin. Consider antibiotic prophylactics for recurrent cellulitis under specialist guidance, e.g. phenoxymethylpenicillin 250mg BD/ erythromycin 250mg BD. Viva Questions: Explain the pathophysiology of cellulitis. Cellulitis is caused by bacteria entering the skin through cuts, bites, or breaks. These bacteria trigger an immune response, causing inflammation, redness, swelling, and pain. Immune cells gather to fight the infection, leading to widened blood vessels and fluid leakage into the tissue (edema). This process can damage the surrounding tissue. If the infection spreads through lymphatic vessels, red streaks may appear, and nearby lymph nodes can become swollen. What are the risk factors of cellulitis? Skin breaks (cuts, bites). Weakened immune system. Impaired circulation. Lymphatic issues. Chronic skin conditions. Obesity. Prior cellulitis. IV drug use. Age-related factors. Unhygienic conditions. Trauma. What are the common pathogens associated with cellulitis? Staphylococcus aureus (including MRSA). Streptococcus pyogenes. Other Streptococci. Other Staphylococci. Haemophilus influenzae (less common). Gram-negative bacteria (in specific cases) What is the Eron Classification for assessing the severity of cellulitis? ree What are the complications of cellulitis? Abscess formation. Bacteremia (bacteria in bloodstream). Lymphangitis (infection spreads via lymphatics). Lymphadenitis (swollen lymph nodes). Necrotizing fasciitis (rare, severe tissue infection). Sepsis (systemic infection). Chronic cellulitis recurrence. Functional impairment and scarring.

Pyelonephritis Doctor Instruction: You are currently a senior surgical doctor on call. Your next patient is Jane – a 35-year-old woman presenting with a fever. Please take a history and perform a relevant examination. Patient History: Jane Doe - a 35-year-old female - office worker. You have been feeling unwell for the past few days. Today you took a temperature which was found to be 38.0 degrees C as you had some shivering. Before the fever started, you remember developing a sudden worsening back pain on the lower left side which is associated with nausea and vomiting (no blood or faecal matter – just food). Pain comes in waves and is sharp – rating it a 7/10 pain score. Your urine also looks darker than usual and smells nasty, with blood in it. You have been going to the toilet more often than usual. You feel unwell. You currently have a poor appetite. Not known to use a catheter. No diarrhoea. No cough. No breathlessness. No flu-like symptoms. No weight loss. No night sweats. Haven't eaten anything abnormal lately. Ideas, Concerns, Expectations: You have no idea what is going on. You think you have an infection but do not know what might be causing it. It might be renal stones. You are concerned because of not feeling your usual self. You want to receive some antibiotics. Past Medical History: High BMI, diabetes type 2 + renal stones (no known urological problems/ procedure in the past) + HIV (positive) Drug History: Metformin NKDA Family History: Renal stones Social History: You live alone in a flat. Ex-smoker – used to smoke 10 cigarettes a day for 10 years. You do not drink. You currently work as an office worker. Examination Findings: Renal angle tenderness (left) + suprapubic tenderness without guarding. No obvious lymphadenopathy. Differentials: Pyelonephritis Cystitis / Urethritis Renal stones / hydronephrosis / post renal problems LUTI Pelvic inflammatory disease/ gynae problems Investigations: Bedside: Observations Pregnancy test (to rule out pregnancy/ectopic) Urine Dipstick /MSU Bloods: Blood sugar level, hba1c (diabetes control due to being a risk factor, FBC/ CRP (raised WBC/ CRP in infection) + U&E (renal function) + LFT / bone profile (baseline / rule out any liver pathology causing high temperature), blood culture Imaging/Special Test: CT KUB (if diagnosis in doubt/ no improvement after 72 hours of treatment/ deterioration) USS KUB (post-renal/ structural abnormalities/ stones) Consider MRI ( in pregnancy/children where renal infection, masses and urinary obstruction are suspected) Consider MCUG (to identify reflux) Consider intravenous pyelogram (small kidneys/ ureteric/ caliceal dilatation/blunting with cortical scarring) Consider renal biopsy (to exclude papillary necrosis – risk is increased ) For recurrent/ chronic pyelonephritis, consider DMSA (to check for scarring and renal damage) Management (Pyelonephritis): Conservative: Rest, hydration, analgesia, /anti-pyrexetics / safety netting / patient education Admit (indication: pregnant women, severe vomiting, relapse of symptoms, inadequate access to follow-up, social issues, non-concordance with treatment, uncertain diagnosis, oliguria/ anuria, urinary tract obstruction, severe pain, dehydration, inability to take fluids/ medication, signs of sepsis, co-morbidities e.g. diabetes) Withhold nephrotoxic medications in acute pyelonephritis Medical: Antibiotics e.g. cefalexin/ co-amoxiclav/ trimethoprim/ ciprofloxacin. (avoid ciprofloxacin/trimethoprim in pregnancy) Initiate sepsis 6 Severe cases: dialysis / renal transplantation Surgery: If the patient does not respond well to treatment, consider renal abscess or kidney stone causing an obstruction. Consider urology referral - surgery to drain renal/perinephric abscesses / to relieve obstructions causing infection e.g. stones / stenting Prevention: Consider prophylactic treatment for those who have symptomatic infection >=3x a year e.g. trimethoprim Viva Questions: Explain the pathophysiology of pyelonephritis. Bacterial Entry: Bacteria, commonly Escherichia coli, enter the urinary tract, often from the urethra, and ascend towards the kidneys. These bacteria multiply, causing infection. Inflammation of Renal Tissue: The bacteria invade the renal parenchyma, leading to inflammation in the renal pelvis and the kidney tissue. Release of Inflammatory Mediators: This invasion triggers an immune response, leading to the release of inflammatory mediators, causing damage to the renal tissues. Obstruction or Reflux: Factors like urinary tract obstructions or vesicoureteral reflux (backward flow of urine from the bladder to the kidneys) can contribute to the persistence and severity of the infection. Symptoms: Patients experience symptoms like fever, chills, flank pain, abdominal pain, nausea, vomiting, and urinary symptoms like frequent urination and pain during urination. Complications: Without proper treatment, pyelonephritis can lead to abscess formation, sepsis, kidney damage, and potential scarring of renal tissue. What are the risk factors of pyelonephritis? Urinary Tract Abnormalities: Structural issues like kidney stones, blockages, or conditions that cause urine to flow backward towards the kidneys (vesicoureteral reflux) increase the risk. Urinary Tract Obstructions: Conditions that hinder normal urine flow, such as an enlarged prostate, tumors, or strictures, can raise the likelihood of infection. Catheter Use: Individuals with urinary catheters are at a higher risk due to the potential for introducing bacteria into the urinary tract. Gender: Women have a higher susceptibility due to shorter urethras, which make it easier for bacteria to enter the urinary tract. Pregnancy: Changes in the urinary tract during pregnancy can increase the risk of urinary tract infections, including pyelonephritis. Weakened Immune System: Conditions or treatments that compromise the immune system, such as diabetes, HIV/AIDS, chemotherapy, or certain medications, can elevate susceptibility to infections. Recurrent Urinary Tract Infections: Individuals with a history of frequent UTIs are at a higher risk of developing pyelonephritis. What are the most common pathogens causing urinary tract infections? The most common pathogens causing urinary tract infections (UTIs) include: Escherichia coli (E. coli): E. coli is the most prevalent bacteria responsible for the majority of urinary tract infections. Staphylococcus saprophyticus: Particularly common in young sexually active females, this bacterium is another frequent cause of UTIs. Klebsiella pneumoniae: This bacterium is known to cause UTIs, particularly in individuals with a compromised immune system. Proteus mirabilis: Commonly found in complicated UTIs, this bacterium is known to form kidney stones and contribute to recurrent infections. Enterococcus species: Enterococci are becoming more prevalent as causative agents of UTIs, especially in healthcare settings. What are the complications of pyelonephritis? Sepsis: The infection can spread to the bloodstream, causing sepsis, a severe and life-threatening condition. Kidney Scarring: Prolonged or recurrent infections can lead to scarring of kidney tissue, potentially affecting kidney function. Kidney Abscess: Formation of abscesses in the kidney, leading to localized collections of pus. Chronic Kidney Disease (CKD): Severe or untreated pyelonephritis can contribute to the development of chronic kidney disease. High Blood Pressure (Hypertension): Kidney damage due to persistent infection can lead to hypertension. Renal Papillary Necrosis: A rare but severe complication causing the death of kidney tissue.