acute care Flashcards
NSAIDS side effects
NSAIDs
CVS – heart failure, stroke Resp - bronchospasm
GI – stomach ulcers
GU – renal failure
Opiods side effects
CNS – drowsiness, hallucinations Resp – respiratory depression (RR<8)
GI – nausea, constipation
GU – urinary retention
Derm – rash (due to histamine release)
Psych – tolerance, dependence, addiction
Naloxonethinking of infection - signs of infection
SLIPR
Swelling
Loss of function
Increased temperature (fever) Pain/ pus
Redness / rigors -> in hospital
Basal Cell Carcinoma
Clinical Features
Clinical Features
• Rolled edge
• Shiny/ pearly appearance • Telangiectasia
• Ulceration (rodent ulcer) • Non-healing
• Can be pigmented
Basal Cell Carcinoma
locations
• Typically present on face
Basal Cell Carcinoma RF
• Risk factors – elderly, UV exposure, immunosuppression, exposure to ionising radiation, arsenic exposure, Xeroderma pigmentosa
Basal Cell Carcinoma management
Management
• Topical agents – 5-fluorouracil and imiquimod • Cryo/radiotherapy
• Excision biopsy / Mohs micrographic surgery
Squamous Cell Carcinoma
RF
Risk factors
- Elderly
- Previous SCC or another skin cancer
- Precancerous (Actinic/solar keratosis & Bowen’s disease
- Outdoor occupation (Sun exposure)
- Fair skin
- Previous cutaneous injury
- Ulcers (Marjolin’s ulcer)
- Inherited conditions (Xeroderma Pigmentosum & albinism)
- Immunosupression
Squamous Cell Carcinoma
Clinical features
Clinical features • Enlarging scaly/crusted lesion • May ulcerate • Grows over weeks to months • Often painful • Located on sun exposed sites
Squamous Cell Carcinoma
Management
Treatment
• Nearly always treated surgical (either excision biopsy or Mohs micrographic surgery)
• Cryotherapy (for very small/low risk) /Radiotherapy (adjuvant/not fit for surgery)
referral for BCC and SCC
Early referral to dermatologist as 2 week wait for SCC/ routine referral for BCC
Causes of CKD
– Diabetes – Hypertension – Glomerulonephritis – Cystic kidney disease – Autoimmune disease (SLE/anti-GBM/vasculitis) – Obstruction/stone disease – Recurrent UTIs – Renovascular disease – Congenital (Alport’s)
Management of CKD:
3 main principles
– Treat the underlying cause e.g immunosuppression
– Prevent progression
• BP and glycaemic control, RAS inhibition
– Manage complications
• Renal anaemia, bone health, managing CV risk, diet
• Fluid overload, uraemia, infection risk
• CKD is defined a
reduced kidney function (eGFR < 60ml/min per 1.73m2) for 3 or more months, irrespective of cause
Clinical Features of Coeliac Disease
Presentation commonest in infants and in 50’s
• Non-specific symptoms (e.g. tiredness, malaise)
• Anaemia
• Nutritional deficiency
• Increased incidence of atopy and autoimmune diseases
• Histology typically shows villous atrophy and crypt hyperplasia with lymphocytic infiltration
Coeliac Disease histology
Histology typically shows villous atrophy and crypt hyperplasia with lymphocytic infiltration
Investigations for Coeliac Disease
FBC shows anaemia (folate/iron deficiency)
• Tissue transglutaminase (tTG) antibodies positive
• Distal duodenal biopsy
• Dual Energy X-ray Absorptiometry (DEXA) – at diagnosis
Management of Coeliac Disease
• Gluten free diet (risk of intestinal T cell lymphoma)
cough acute subacute chronic timeframes
Acute: < 3 weeks
Subacute: 3-8 weeks Chronic: > 8 weeks
cough history
Most important 2 questions:
- How long have they had the cough?
- Is it productive or dry? Haemoptysis? ▪ Pattern to cough?
- Nocturnal (Asthma, GORD, UACS, pulmonary oedema)
- On exercise (asthma/cough variant asthma)
- Environments (asthma, hypersensitivity pneumonitis, UACS)
▪ Associated symptoms? - URTI symptoms
- Shortness of breath (et change, progression, pattern)
- Systemic sx: fevers (pneumonia, tb), night sweats or weight loss (lung ca, tb) - Pleuritic chest pain
- Heart burn or reflux
cough acute DDX
productive - Bronchitis
Pneumonia
dry - URTI
Asthma/COPD
Drug induced
Congestive heart failure Smoke/toxin inhalation
PE
Hypersensitivity pneumonitis Pericarditis
cough Subacute (3 – 8 weeks) ddx
productive -
Pneumonia
dry Post infectious Pertussis
cough investigations
Investigations
▪Anyone with red flag symptoms or persistent chronic cough need formal investigation ▪Spirometry (restrictive vs obstructive)
▪ CXR
▪If productive sputum mcs. RVS w/ PCR. ▪Bloods – FBC, CRP, LFTs, Renal profile. ▪CT Chest
▪BNP +- Echo
▪Manometry/OGD
▪Bronchoscopy
▪Bronchial provocation test
▪QuantiFERON-TB gold/ T-spot test, BD Glucan, galactomannan antigen test, Vasculitic screen, AI screen
Cushing’s Syndrome
causes
ACTH Dependent - pituitary tumour, small cell lung cancer, carcinoid tumour
ACTH Independent
Steroids
Adrenal adenoma
Adrenal Carcinoma
Cushing’s Syndrome presentation
Signs and symptoms: • Moon face • Buffalo hump • Truncal obesity • Thin skin/easy bruising/striae • Osteoporosis/fractures • Reduced inflammatory and immune response • Rhabdomyolysis • Vasoconstriction and water retention • Reduce GnRH
Cushings Investigations
Exclude exogenous causes! 24h urinary free cortisol level
Cushing’s syndrome possible if result is positive (>50 mcg/24h), need additional investigations. Test twice on separate days for diagnostic reliability.
Low dose dexamethasone suppression test (1mg)
Cushing’s syndrome likely if results positive (morning cortisol >1.8 mcg/dL) combined with positive 24h urinary free cortisol level. Rule out false positives.
High dose dexamethasone suppression test (8mg)
Cushing’s syndrome confirmed if positive (cortisol <50% of baseline) and suggests pituitary cause.
Plasma ACTH
Determine if etiology of Cushing’s syndrome is ACTH dependent or independent. Pituitary or ectopic cause if >20 picograms/mL. Adrenal cause if <5 picograms/mL
Pituitary MRI/Adrenal CT
Treatment bushings
Treat primary cause of Cushing’s Syndrome
Surgical treatment
• Transsphenoidal pituitary adenectomy
• Adrenalectomy
• Surgical resection of tumour
• +/- chemo/radiation therapy
Medical treatment
• Somatostatin analogue: Pasireotide
• Adrenal steroid inhibitors: Ketoconazole, Metyrapone
• Glucocorticoid receptor antagonist: Mifepristone
• Post-surgical/radiation corticosteroid replacement therapy
phaeochromocytoma is a rare catecholamine secreting tumour.
clinical features
Features are typically episodic hypertension (around 90% of cases, may be sustained) headaches palpitations sweating anxiety
Phaeochromocytoma investigatios
Tests
24 hr urinary collection of metanephrines (sensitivity 97%*)
this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)
Phaeochromocytoma management
Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)
seizure history
Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)
Status Epilepticus
management
Management (NICE) Stage 1 - 0-10mins: • Secure airway • High flow O2 • Assess A-E • IV access if possible • First dose of benzodiazepine (PR diazepam/IV lorazepam)
Stage 2 (11-29mins) • Regular observations • Repeat benzo dose if indicated
Stage 3 - Established Status Epilepticus (30- 60mins)
• Phenytoin and/or phenobarbital infusion
• Call anaesthetics/ITU –> ?intubation
Traumatic Brain Injury patient in ER Resuscitation and evaluation
ABCDE (ATLS guideline) > Special attention to hypoxia and hypotension.
GCS 8 or less > involve anesthetist or critical care physician to provide appropriate airway management.
Clotting function should be checked and corrected.
Traumatic Brain Injury patient in ER
Primary investigation of choice
: CT imaging of the head
Head injury
Indications of CT imaging within 1 hour:
Indications of CT imaging within 1 hour:
- CGS <14 at any point.
- GCS <15 at 2 hours.
- Focal neurological deficits.
- Suspected open, depressed or basal skull fracture.
- More than one episode of vomiting.
- Post-traumatic seizure.
Head injury
Indications within 8 hours:
Indications within 8 hours:
- Age >65
- Coagulopathy (aspirin, warfarin or rivaroxaban use) - Dangerous mechanism of injury (fall from hight, RTA) - Retrograde amnesia >30 minutes.
Cardinal signs of brain compression and herniation
1) Contralateral hemiparesis (compression of corticospinal tract in midbrain)
2) Decreasing GCS (involving reticular system)
3) Ipsilateral pupillary dilatation (compressed parasympathetic fiber of oculomotor nerve at tentorial hiatus)
Causes of Delirium - PINCHME
Pain (or pain-killers – opioids in AKI), palliative, post-surgical, trauma/bleed*
• Infection (UTI, Chest infection, Cellulitis or Sepsis), isolation
• Nutrition, Night pattern (sleep cycle), Noise (too quiet/loud)
• Constipation, Continence (new change)
• Hydration status, hyper(metabolic/endocrine), hypo(metabolic/endocrine/ fluid/electrolyte imbalance), hallucinations
• Medication (polypharmacy/concordance/ substance abuse*), mobility
• Environment (over/under stimulation), Emotional (stressors)
delirium Investigations
- History – collateral Hx
- Examination - thorough
- FBC, U+Es, LFTs, CRP
- Glucose
- TFTs
- Magnesium, Calcium Phosphate
- B12, folate, iron studies
- ABG if desaturating
- CXR
- MSU (DO NOT DO URINE DIP AS A POSTIVIE DIP DOES NOT MEAN THAT THEY HAVE AN INFECTION)
- ECG
Management of Delirium
• Effective communication and • re-orientation • Reassurance by involving family and friends • Stable environment • 1:1 nursing if at risk of falls
Treat underlying cause
• Stop medications
• Reduce Anticholinergics
• Sedate with lorazepam – 1- 2mg at night (IM/Oral) – peak effect 90mins
• Optimise visual and auditory • acuity
• Non-verbal communication
• Do not argue or correct
delusions
• Temporary physical restraints
In dementia, can give olanzapine 2.5mg ON (max dose 10mg), alternatively can give risperidone (increases cardiac/stroke events)
• Haloperidol 0.5mg-1mg is the last resort
MMSE
As per NICE : • Normal 25 or more • Mild Impairment 21-24 • Moderate Impairment 10-20 • Severe Impairment <10
dementia investigation
Cognitive tests: MMSE (≤23/30), Addenbrookes (ACE), MoCA Bloods: FBC, U+Es, TFTs, B12/folate, Ca2+
Imaging: CT, MRI, functional neuroimaging
Biochemical features of HypoPT
hypocalcemia
hyperphosphatemia
low or inappropriately normal levels of parathyroid hormone (PTH)
hypercalciuria
hypernaterium causes
Hypovolaemic Renal loss of Na urine Na >20 mmol/day Diuretic use Salt wasting nephropathy Mineralocorticoid deficiency/adrenal insufficiency Renal tubular acidosis Extrarenal(renal conservation ) urine Na <20 mmol/day Burns Gastrointestinal loss Pancreatitis Blood loss
Euvolaemic : Thiazide diuretics (can be euvolaemic or hypovolaemic) Hypothyroidism Adrenal insufficiency (can be euvolaemic or hypovolaemic) SIADH
Hypervolaemic
Congestive cardiac failure Cirrhosis
Nephrotic syndrome
Syndrome of Inappropriate Anti Hormone secretion (SIADH)
criteria
Essential criteria –Rule of 3
◦ osmolality –Urine > 100 & serum < 275 mOsm/kg
◦ Urine Na 30 mmol/l
◦ No other causes -Absence of adrenal, thyroid, pituitary or renal insufficiency, Diuretics
Causes of SIADH
Malignant disease Bronchogenic carcinoma Pulmonary disorders Viral and bacterial pneumonias Tuberculosis Neurologic disorders Encephalitis Meningitis Trauma Stroke Alcohol withdrawal Other HIV/AIDS Acute psychosis Acute intermittent porphyria Idiopathic
Primary Polydipsia
Psychiatric disorder, often complicated by increased thirst with antipsychotic meds
can occur with hypothalemic lesions (sarcoid or other infiltrative processes)
Usually no hyponatremia unless intake over 10-15 L/day, or acute 3-4 L water load
Urine osm below 100 (NOT ADH problem!)
Increased problems if other ADH stimulus (n/v, anxiety)
Treatment hyponatremia
Fluid restriction – 1 L per day or less
Hypertonic saline – If severe
Medications
◦ Demeclocycline –( a tetracycline derivative) - inhibits cyclic AMP, which diminishes the intracellular effects of ADH on the renal tubular cells
◦ Vaptans - vasopressin-2 receptor antagonists – (Tolvaptans )
Produces selective diuresis ( Aquaresis) with no effect on K & Na
total anterior circulation stroke
ALL THREE
unilateral weakness of face, arm and leg
homonymous hemiopoea
higher cerebral dysfunction
Partial anterior circulation stroke
two or more of
unilateral weakness of face, arm and leg
homonymous hemiopoea
higher cerebral dysfunction
lacunar stroke
one of
pure sensory stroke
pure motor stroke
ataxic hemiparseis
post thromblysis care
monitor - GCS, pulse and BP every 15 mins for 2 hours and then 30 mins for next 6
after if no haemorrhage start aspirin 300mg
stroke not in anticoagulant window
300 mg once daily for 14 days, before being considered for anticoagulant treatment.
post stroke clopidogrel not tolerated
If clopidogrel is contraindicated or not tolerated, given aspirin and modified release dipyramidole for secondary prevention following stroke
Barthel index
The Barthel index is a scale that measures disability or dependence in activities of daily living in stroke patients
standard target time for thrombectomy
The standard target time for thrombectomy in acute ischaemic stroke is 6 hours
‘Young’ stroke blood tests
thrombophilia and autoimmune screening - performed in those under 55 with no obvious cause of a stroke
Anterior cerebral artery
Contralateral hemiparesis and sensory loss, lower extremity > upper
Middle cerebral artery
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
Posterior cerebral artery
Contralateral homonymous hemianopia with macular sparing
Visual agnosia
Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain)
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)
Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus
• Murphy sign
in acute cholecystitis pain is experienced by the patient on inspiration (liver & gall bladder pushed downward) when an examiner’s hand is pressed towards the right upper quadrant due to the inflammed gall bladder hitting the examining hand.
Boas sign
in acute cholecystitis there is an area of hyperaesthesia between 9th - 11th ribs below the tip of right scapula elicited by stroking the skin in that area.
Rovsing sign
in acute appendicitis palpation of the left iliac fossa causes pain the the right iliac fossa.
Grey Turner’s sign
Flank bruising due to blood tracking into the
retroperitoneal plane from haemorrhagic pancreatitis or rupture of abdominal or iliac aneurysm.
Cullen’s sign
Periumbilical bruising due to haemorrhagic pancreatitis,
ruptured ectopic pregnancy r other causes of haemoperitoneum.
Intestinal obstruction presentations
Vomiting (early in small bowel obstruction cf large bowel obstruction) • Vomiting of food – obstruction above 2nd part of duodenum
• Vomiting of bile – obstruction below 2nd part of duodenum
• Abdominal pain - colicky
• Abdominal distension
• Absolute constipation – unable to pass flatus or motions
can be mechanical or adynamic
Features of strangulation in obstruction
Mechanical obstruction symptoms sudden & pronounced
• Continuous pain or dull ache between colic
• Localised to region of affected bowel
• Localised tenderness
• Guarding, no bowel sounds, tachycardia
General post-operative complications
- Nausea
- Hiccups
- Headaches
Post–op pulmonary complica
Pulmonary collapse • Pulmonary infec9on • Respiratory failure • ARDS • Pleural effusion • Pneumothorax • Stop smoking pre-op
Post-op cardiac complications
Myocardiac ischaemia /infarction • Cardiac failure • Arrhythmias • Post-operative shock • Management • Exclude surgical complications as causes
Post-op thromboembolism
- DVT
- Anti-thromboembolism measures • TED stockings
- Subcutaneous heparin
- Intra-operative calf-pumps
- Pulmonary embolism
- History of DVT
- Hip operations
- Anti-thrombin III deficicency; Protein S def; Protein C def
Post-op urinary complications
Urinary retenFon
• Post hernia repair, anorectal surgery, prostaFsm • UTI
• Urinary catheter, urethral instrumentaFons
• Renal failure
• Fluid/blood loss, jaundice (hepatorenal syndrome),
hypotension/shock, nephrotoxic drugs
Post-op cerebral complica9ons
- CVA
- Neuropsychiatric complications • Delirium tremens
- Post TURP syndrome
Post-op pyrexia
At 1-2 days • Physiologicalresponsetosurgery • Pulmonarycollapse,atelectasis At 3-5 days • Woundinfection • Intra-abdominalcollection • Chestinfection • Catheter/centrallinerelatedinfection At 5-7 days • Anastomoticdehiscence,DVT After 7 days • Sepsis–intra-abdominalcollection/othersources
Hartmann’s procedure
Indications
Resect pathology in sigmoid colon: end colostomy and closure of rectal stump • DiverIcular inflammatory mass / abscess / fistula • DiverIcular perforaIon • DiverIcular haemorrhage • Sigmoid carcinoma • ObstrucIon • PerforaIon • Sigmoid volvulus • ColiIs • Massive colonic haemorrhage
Splenectomy: complica?ons
- Post-op
- Bleeding
- Pancreatic injury
- Pulmonary complications • Thrombotic complications • Subphrenic abscess
- Late
- Overwhelming sepsis
- Prophylactic antibiotics
Laparoscopic cholecystectomy
Early complications • Bleeding • Bile leak • Damage to common bile duct Late complications • Retained stones • Bile duct stricture
Nissen fundoplication
for GORD
ost-op complications • Too tight a fundoplication
• Unable to burp / vomit • Recurrence of reflux
Gastrectomy complications
•
Gastrectomy complications • Early • Anastomotic leak • Bleeding • Delayed gastric emptying • Late • Iron def anaemia • B12 deficiency • Hypocalcaemia • Carcinoma
Dumping syndrome - Osmotic effect due large amount of food enters into the jejunum
Right hemicolectomy
remove the right-hand portion of the colon (approximately half the colon). This will include the caecum, ascending colon and a portion of the transverse colon.
Left hemicolectomy
the descending colon is removed. This is the part of your colon that’s attached to your rectum. After it’s removed, the surgeon attaches the transverse colon directly to your rectum
Ileopouch anal anastomosis IPAA indications
Ulcerative colitis
• Familial adenomatous polyposis coli (FAP)
Stomas
Ileostomies
• Loop
• End
Colostomies
• Loop
• End
• Double barrel
Ileostomies
loop = loop ileostomy is typically temporary and performed to protect a surgical join in the bowel.
End - large bowel (colon) is removed-and the end of your small bowel is brought to the surface of the abdomen to form a stoma. (if permanent - Ulcerative colitis or familial adenomatous polyposis)
They are typically located in the right iliac fossa (RIF).
Less water is absorbed in the small bowel so the contents of the stoma bag tend to have a liquid consistency.
Because the enzymes contained in small bowel contents can irritate the skin, the bowel has a spout sticking out from the abdominal wall. This allows faeces to drain without touching the skin.
colostomies - made using the large bowel (or colon).
flush to the skin (i.e. no spout) because the enzymes present in large bowel contents are less alkali and therefore less irritating to the skin.
main risk factor for cholangiocarcinoma
PSC
Epididymal cysts
Features
separate from the body of the testicle
found posterior to the testicle
Associated conditions
polycystic kidney disease
cystic fibrosis
von Hippel-Lindau syndrome
Diagnosis may be confirmed by ultrasound
preferred diagnostic test for chronic pancreatitis
CT pancreas with IV contrast
Postoperative ileus
Disruption of the normal coordinated movement of the GI tract following (abdominal or non abdominal) surgery
Physiological post op ileus – generally benign, self-resolving (0-72h)
Prolonged – suggested ileus >5d abnormal (40% of patients following laparotomy)
Aetiological inf lammatory, pharmacological (opioids), hormonal (stress response)
Abdo pain, bloating, nausea and vomiting, may or may not continue to pass flatus and stool
Management: NG tube for decompression if required, iv fluids, slowly introduce oral intake (chewing gum/sweets), correct electrolyte imbalances, early mobilisation and wean off opioids
incisional hernia management
Surgical repair with mesh
Recurrence - up to 50% of large hernias
or conservative - think of patient health and wellbeing
four cardinal features of intestinal obstruction:
Vomiting (faeculent)
Colicky pain (tinkling bowel sounds) Constipation
Abdominal distension
Small v large bowel obstruction:
Small bowel obstruction Vomiting occurs earlier Distension less Pain higher in abdomen Absolute constipation less likely Large bowel obstruction Vomiting occurs later Distension more Pain lower in abdomen Absolute constipation more likely
Ileus v mechanical obstruction
Ileus
No pain
Tinkling bowel sounds absent
Obstruction
Pain
Tinkling bowel sounds present
Simple/closed loop/strangulated obstruction
Simple-one obstructing point with no vascular compromise
Closed loop-obstruction present at two points, forming a loop of grossly distended bowel at risk of perforation
Strangulated-Blood supply compromised. Peritonism the cardinal feature.
General principles of management of obstruction
mmediate action: NBM, NGT, IV fluids, correct electrolyte imbalance, analgesia, AXR, CXR, bloods
Further imaging:
Colonoscopy in instances of suspected mechanical obstruction
Water soluble contrast (diagnostic and therapeutic)
Surgery:
Dependent on multiple factors. Strangulation/closed loop obstruction and large bowel often require surgery
Caecal volvulus
Investigations: AXR, contrast enema, CT Treatment:
Colonoscopic decompression (if unfit for surgery) Reduction alone
Right hemicolectomy
Caecostomy
Caecopexy
78yo F c/o PR bleed with associated dizziness & abdo pain…DDX
Haemorroids fissure polyps colitlis carcinoma Angiodysplasia
Management of acute LGI bleed
. ABC resuscitation
2. History & examination
3. IV access with 2x large bore cannulae & take bloods for FBC, clotting, renal function, crossmatch >2-4units
4. Fluid management – commence IV fluids (consider transfusion), monitor UO via catheter
5. Regular obs & commence stool chart
6. If bleed is persistent, massive &/or progressive then
consider urgent angiogram or surgery
7. Identify site & cause of bleeding for further management
PE presentation
Sudden-onset shortness of breath, pleuritic chest pain, and haemoptysis (this is the ‘typical’ triad, although note that all three features are rarely present).
A massive pulmonary embolism may present with the above and syncope/shock.
A small pulmonary embolism may be asymptomatic.
