Week 13 OBGYN Flashcards
Lymphangitis
Red, warm streak lines along arm or leg from the infected area towards a group of lymph nodes. The nodes become enlarged and feel tender. Fever, chills, rapid heart rate, headache. Typically staph aureus.
Superficial vein thrombosis/thrombophlebitis
Most commonly the saphenous vein. Involves thrombus with inflammation surrounding the vein. Pain, tenderness, itching, redness, hardened skin overlying. DVT or PE can be associated with it. Can also get infection, hyperpigmentation, subcutaneous nodule, varicose veins. Uncomplicated = self resolving within two weeks.
NSAID, warm compress, elevation, exercise, compression stockings, think of possible coagulation disorder. Low molecular weight heparin and fondaparinux reduce risk of extension or reoccurrence.
Scabies
Itchy skin condition by parasitic burrowing mite called sarcoptes scabiei hominis. Often direct skin contact spreads. Sometimes sexually transmitted or by linen.
Itchy at night, on trunk and limbs. Sometimes not if it is crusted. Itch can stay for a few weeks after treatment. Like the spaces between fingers, palms and wrists. Also found in elbows, nipples, buttocks, penis, insteps and heels. Rash has varied appearances as red papules in follicles, dermatitis, vesicles, actopustulosis, papules or nodules in intimate places. Often red, dotty or lumpy.
Can get secondary staph or strep infections leading to plaque and pustule impetigo. Staph cellulitis makes painful redness, swelling and fever. Can also give post strep glomerulonephritis and acute rheumatic fever.
Crusted scabies = very contagious. Much more infested. Yellow-white crust. Can affect scalp. Can raise IgE and eosinophilia.
Home is treated with insecticide. Scabs ideas are applied head to toe. 5% permethrin cream left on the skin 8-10 hours. Use nail brush to get it under nails. Can also use oral ivermectin. Repeat the treatment after 8-10 days for newly hatched mites.
Septic arthritis
Infection of joint capsule. Commonly staph aureus. Can also be gonoccocal arthritis- more common in elderly. Revised prosthetic joints, old age, dm, prior joint damage, immunodeficiency = at risk.
Single warm, swollen joint, painful on passive movement. Often have fevers and rigours. If bacteraemia- prostration, vomiting or hypotension. If septic at sternoclavicular, acromioclavicular, sternocostal or manubrosternal joints can have chest wall pain instead. Infection of sacroiliac is buttock, hip or anterior thigh pain. Most commonly the knee. Then hip, shoulder then wrist.
Gout or pseudogout can also present with pain, inflammation, spiked fevers and chills.
Septic shoulder is more commonly group B strep. Gonococcal disease presents with fever, arthralgia, multiple skin lesions as dermatitis-arthritis syndrome and tendinosynovitis of hand joints, knee, wrists and elbows. Not always, can be monoarticular.
Lyme disease can cause swelling disproportionate to pain. Can appear in joint months after infection.
Give surgical draining and antibiotics. Iv for 2-3 weeks then oral 2-4 weeks. Flucloxacillin or Clindamycin if allergic. If MRSA, give vancomycin or teicoplanin. If gonococcal, give cefotaxime or ceftriaxone for two weeks. If strep B is resistant, give penicillin and gentamicin or 3-4 gen cephalosporin. Splint the joint. Might need aspiration.
Endocarditis
Inflammation of endocardium, often at heart valves. Characterised by vegetation = mass of platelets, fibrin, micro colonies and inflammatory cells. Can granulate if subacute. Can be infective or non infective. Get echo and blood cultures.
Signs are fever, chills, Roth spots, sweating, weakness, weight loss, splenomegaly, murmur, hf, petechia, oslers nodes, Jane way lesions.
Commonly strep or staph. Non infective causes are lupus, hyper coagulation, venous catheters, adenocarcinoma.
Lung abscess
Necrosis of pulmonary tissue and formation of cavities full of necrotic debris or fluid from microbial infiltration. Also called necrotising pneumonia. Symptoms chest pain more when breathing in, cough, fatigue, fever, night sweats, pus and sputum mixed with bad smell, sour or bloody. Cachectic, clubbing. Local dullness on percussion and bronchial breathing sounds.
Can be caused by septic emboli, aspiration from GI, necrotising pneumonia, granulomatosis with polyangiitis or vasculitis.
Some will self resolve. Give antibiotics. Can be predisposed by alcoholism. Often staph.
Gas Gangrene
Clostridial myonecrosis caused by clostridium perfringens anaerobes from soil. Exotoxins destroy muscle tissue and produce gas. Edematous, necrotic bullae, crepitation from gases escaping the tissue. Symptoms also include foul, sweet discharge, fever, pain, tachycardia, numbness, jaundice. Treatment is debridement, excision, amputation, antibiotics.
Anthrax
Infection of bacillus anthracis. Can be on skin, lungs, intestine and iv drug site. Blister turns to ulcer with black center, painless. If inhaled has fever, chest pain and shortness of breath. An abscess can develop. Doesn’t usually spread between people. Infected by inhaling or broken skin contact to spores. Give anthrax vaccination or antibiotics.
Cutaneous form is known as hide porters disease. The lesion is itchy. Appears 2-5 days after infection. Nearby lymph nodes can swell.
Lung anthrax looks like cap. Begins with haemorrhaging mediastinitis. Pneumonia occurs when it spread via lymph nodes into the lung tissue
GI anthrax is from infected meat.
Pos purple rods
Hep C treatment
Pegylared Interferon and ribavirin
Endopthalmitis
Endophthalmitis is severe inflammation of the anterior and/or posterior chambers of the eye. Whilst it may be sterile, usually it is bacterial or fungal, with infection involving the vitreous and/or aqueous humours.
Most cases are exogenous and occur after eye surgery (including cataract surgery) or penetrating ocular trauma, or as an extension of corneal infection. An increasing number of cases are occurring after intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) medications. Endophthalmitis may also be endogenous, arising from bacteraemic or fungaemic seeding of the eye.
Acute bacterial endophthalmitis is a medical emergency, because delay in treatment may result in vision loss.
When inflammation spreads throughout the globe and involves all the layers ± the peri-ocular tissues, the condition is known as panophthalmitis.
The most common pathogens in endophthalmitis vary by cause:
Coagulase-negative staphylococci are the most common causes of post-cataract endophthalmitis.
Coagulase-negative staphylococcal bacteria and viridans streptococci cause most cases of post-intravitreal anti-VEGF injection endophthalmitis.
Bacillus cereus is a major cause of post-traumatic endophthalmitis.
Staphylococcus aureus and Streptococcus spp. are important causes of endogenous endophthalmitis associated with endocarditis.
In Southeast Asia, Klebsiella pneumoniae causes most cases of endogenous endophthalmitis, in association with liver abscess.
Endogenous fungal endophthalmitis in hospitalised patients is usually caused by Candida spp., particularly Candida albicans.
Presentation is usually acute, with eye pain and decreased vision.
The eyelid may be swollen (about one third of cases)
Occasionally the condition is not painful.
Hypopyon is a common finding, and the appearance of the eye may be hazy.
In exogenous endophthalmitis, infection is confined to the eye. There is no fever and minimal, if any, peripheral leukocytosis.
Discitis
Discitis is inflammation of the vertebral disc space. It is usually associated with infection and can co-exist with vertebral osteomyelitis (spondylodiscitis).
It most commonly affects the lumbar spine. The thoracic spine is least commonly affected with the cervical spine between the two.
There is usually haematogenous spread of infection from other parts of the body. The urinary tract, lungs and soft tissues are common primary sites for infection. It may be difficult to find a primary site.
Staphylococcus aureus is the most common pathogen.
Discitis can occur in children but most commonly affects males aged in their 50s.
Risk factors include any cause of immunosuppression (including diabetes) and intravenous drug use.
Discitis may rarely follow surgery involving the disc space.
Presentation
Diagnosis is difficult and often delayed or missed due to the rarity of the disease and the high frequency of low back pain in the general population.
An insidious onset is common, with neck or back pain and localised tenderness. Pain is worse on movement. Mobility may be restricted.
There may be associated fever and weight loss.
Neurological deficit may be present. This is more likely in the cervical spine.
Antibiotics are needed. These should be adjusted if/when culture results are available. Parenteral treatment is usually used and may be needed for 6-8 weeks. ESR can be used to monitor response.
Immobilisation: two weeks of bed rest have been suggested, followed by immobilisation with a brace, which may be needed for 3-6 months.
Analgesia should be prescribed as required.
Surgical treatment may be needed if there is neurological deficit, spinal deformity or lack of response to antibiotic treatment.
Prolapsed disc
The nucleus pulposus of the disc is usually contained by the annulus fibrosus. If the nucleus herniates, it can irritate and/or compress the adjacent nerve root, causing symptoms of sciatica.
A herniated nucleus pulposus is most common in those aged below 40 years, whilst degeneration of discs tends to affect those aged over 40 years
.
About 90% of cases of sciatica are caused by a herniated intervertebral disc. This most commonly occurs at the L5/S1 level.
Lumbosacral disc herniation
If there is nerve entrapment in the lumbosacral spine, this leads to symptoms of sciatica which include:
Unilateral leg pain which radiates below the knee to the foot/toes.
The leg pain being more severe than the back pain.
Numbness, paraesthesia, weakness and/or loss of tendon reflexes, which may be present and are found in the same distribution and only in one nerve root distribution.
A positive straight leg raising test (there is greater leg pain and/or more nerve compression symptoms on raising the leg).
Pain which is usually relieved by lying down and exacerbated by long walks and prolonged sitting.
Large herniations can compress the cauda equina, leading to symptoms/signs of saddle anaesthesia, urinary retention and incontinence as described above.
Symptoms tend at least to resolve partially in 66% of people with a disc herniation, after six months. This is because the herniated portion tends to regress over time
Thoracic disc herniation
Disc lesions in the thoracic spine can lead either to nerve root irritation or to cord compression.
Thoracic spine lesions can present with symptoms similar to lumbar disc lesions.
In nerve root irritation, there may be shooting pain down the legs.
There may be pain, paraesthesia or dysaesthesia in a dermatomal distribution.
A thoraco-abdominal sensory examination can help to determine the level of the lesion: the nipple is innervated by T4; the xiphoid by T7; the umbilicus by T10; the inguinal region by T12.
Testing of the abdominal and cremasteric reflexes can help to identify myelopathy and cord compression.
Cord compression:
This is a neurosurgical emergency.
Cord compression in the thoracic spine can produce paraplegia.
There may be clonus or a positive Babinski reflex.
There may be bladder/bowel dysfunction.
Herniation of T2-T5 can mimic cervical disc disease.
Simple analgesics as first line (paracetamol/non-steroidal anti-inflammatory drug). These may be used in combination.
A weak opioid such as codeine or tramadol may be added if pain is still present.
Consider a benzodiazepine (eg, diazepam) if there is muscle spasm.
Consider a trial of a tricyclic antidepressant or gabapentin if there is persistent sciatica.
If stronger analgesia is needed, refer to a pain clinic/specialist service.
Encouragement to keep active: swimming is a good exercise.
Heat and massage may relieve muscle spasm.
Avoidance of activities that may aggravate pain - eg, lifting, prolonged sitting.
Physiotherapy.
Surgery:
Pain due to a herniated lumbosacral disc may settle within six weeks. If it does not, or there are red flag signs such as the possibility of cauda equina syndrome, referral to an orthopaedic surgeon or a neurosurgeon should be considered.
Post-partum haemorrhage
4Ts- thrombocytopenia, tears, atonic uterus, retained placental tissue. Atony- uterus doesn’t contract and neither do exposed vessels where the placenta has been . Give IM syntocinon, bimanual compression, iv syntometrine, tranexamic acid 1g slow IV.
Reserve cell salvage and blood products and hysterectomy. Retained tissue should be removed and tears repaired.
Shoulder dystocia
x happen with multiples. Baby’s head is turtle necking/bobbing as shoulder is stuck on pubic bone. Risk brachial plexus injury- bell’s or erb’s palsy or brain damage.
Place mother in McRoberts position to ease pelvis wider. Apply suprapubic pressure. This usually works.
Give episiotomy for hand space- pringle hand position under chin and swoop. Can deliver arm first or rotate the shoulder in corkscrew manuvre.
Can also break baby’s collarbone or mother’s pubic bone to make space.
Can push the baby back up into the uterus and risk uterine rupture for emergency caesarean.
Hyperemesis Gravidarum
Nausea and vomiting of pregnancy (NVP) normally starts between 4 and 7 weeks’ gestation. It reaches a peak in the 9th week, and settles by week 20 in 90% of women.
Hyperemesis gravidarum (HG) is diagnosed when there is prolonged and severe NVP with:
More than 5% pre-pregnancy weight loss
Dehydration, and
Electrolyte imbalances.
It is thought to be due rapidly increasing levels of beta human chorionic gonadotrophin (hCG) hormone, which is released by the placenta. High hCG stimulates the chemoreceptor trigger zone in the brainstem, which feeds into the vomiting centre of the brain.
The risk factors for developing hyperemesis gravidarum include:
First pregnancy Previous history of hyperemesis gravidarum Raised BMI Multiple pregnancy Hydatidiform mole
Moderate (or cases where community management has failed) – should be managed with ambulatory daycare. This involves IV fluids, parenteral antiemetics and thiamine. The patient should be managed until ketonuria resolves.
First line:
Cyclizine
Prochlorperazine
Promethazine
Chlorpromazine
H2 receptor antagonists or proton pump inhibitors: for reflux, oesophagitis or gastritis
Thiamine: for prolonged vomiting to prevent Wernicke’s encephalopathy
Thromboprophylaxis: for all women requiring admission- clexane.
