acute and emergency Flashcards

presentation and conditions (379 cards)

1
Q

Haematuria

A

-Microscopic or dipstick positive haematuria is increasingly termed non-visible haematuria

-Macroscopic haematuria is termed visible haematuria.

-Non-visible haematuria is found in around 2.5% of the population.

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2
Q

What are the causes of SPIRIOUS non-visible haematuria

A

-urinary tract infection
-menstruation
-vigorous exercise (this normally settles after around 3 days)
-sexual intercourse

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3
Q

Causes of PERSISTANT non-visible haematuria

A

-cancer (bladder, renal, prostate)
-stones
-benign prostatic hyperplasia
-prostatitis
-urethritis e.g. Chlamydia
-renal causes: IgA nephropathy, thin basement -membrane disease

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4
Q

Spurious causes - red/orange urine, where blood is not present on dipstick

A

-foods: beetroot, rhubarb
-drugs: rifampicin, doxorubicin

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5
Q

Testing for haematauria

A
  • We do not screen for haematuria as it’s very ccommon

Investigations
- urine dipstick is the test of choice for detecting haematuria

-persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart

-renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked

-urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected

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6
Q

When urgent referral is needed for non-visible haematauria

A

Aged >= 45 years AND:
-unexplained visible haematuria without urinary tract infection, or

-visible haematuria that persists or recurs after successful treatment of urinary tract infection

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test

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7
Q

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test- what are the likely diagnosis

A
  • UTI
  • Bladder Cancer
  • Prostatitis
  • Renal Parenchymal Disease
    -Benign Prostatic Hyperplasia (BPH)
    -Kidney Stones
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8
Q

Differential diagnosis Aged >= 45 years AND:
-unexplained visible haematuria without urinary tract infection, or

-visible haematuria that persists or recurs after successful treatment of urinary tract infection

A
  • Urinary Tract Stones (Nephrolithiasis or Urolithiasis)
  • bladder cancer
    -Exercise-Induced Hematuria:
    -Renal Trauma or Injury
    -Medication-Induced Hematuria
    -Coagulopathy or Bleeding Disorders
    -Renal Parenchymal Disease
  • Renal bladder stones
    -UTI
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9
Q

Reasons for non-urgent referral when haematauria is discovered

A

Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection

patients under the age of 40 years with normal renal function, no proteinuria and who are normotensive do not need to be referred and may be managed in primary care

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10
Q

Nephrotic syndrome and the four signs of it

A
  • Kidney disorder where there is damage done to the glomeruli.
  • ## large amounts of protein leaking into the urine.1.Proteinuria:

2.Hypoalbuminemia

  1. Edema.
  2. Hyperlipidemia
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11
Q

What are risk factors for suicide?

A
  • mental health conditions
  • previous suicide attempts
  • family history
  • stressful life hx
  • access to means
  • chronic illness
  • males are more likely
  • making efforts not to be found
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12
Q

Anaphylaxis

A
  • life-threatening allergic reaction which occurs in minutes after exposure to a trigger

Symptoms
- swelling of the lips, mouth, throat and tongue
- rash on the body
- Difficulty breathing
- unconscious

typically for anaphylaxis to be diagnosed, 2/4 conditions need to be diagnosed with

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13
Q

Managment of anaphylaxis

A

ALL AGES NEED A-E MANAGEMENT

-Children weighing 15-30 kg: 0.15 mg (0.15 mL)
-Children weighing >30 kg: 0.3 mg (0.3 mL)
- Adults (0.5ml of 1:1,000 adenaline)

Antihistamines (e.g., cetirizine, diphenhydramine) and corticosteroids (e.g., hydrocortisone) may be given to help relieve symptoms and prevent recurrence.

Nebulized bronchodilators (e.g., salbutamol) may be used for severe respiratory symptoms.

Refer to allergy clinic where 2 epi-pens and training need to be given.

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14
Q

Sepsis

A

Sepsis is a life-threatening condition that occurs when the body’s response to an infection causes widespread inflammation, leading to organ dysfunction and failure.

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15
Q

Sepsis 6 (BUFALO)

A

take 3/give 3

take
- Bloods
-Urea
-Lactate

Give
- Fluids
-Oxygen
- Antibiotics

BUFALO
-Bloods
-Urea
Fluids
-Antibiotcs
-Lactate
-Oxygen

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16
Q

what are the symptoms of Sepsis

A
  • Decreased Urine output
  • low blood pressure
  • fever
  • tachycardia
  • tachypnoea
  • altered mental status
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17
Q

causes of sepsis

A
  • UTI
  • pneumonia
  • abdo infections
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18
Q

complications of Sepsis

A

-ARDS
-DIC
- Multiple organ failure
- acute kidney injury

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19
Q

Criteria for sepsis

A

Sequential Organ Failure Assessment (SOFA) score and the quick SOFA (qSOFA) score are commonly used to assess the severity of organ dysfunction and predict outcomes in sepsis.

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20
Q

Neutropenic sepsis

A

Neutropenic sepsis, also known as febrile neutropenia, is a medical emergency characterized by the presence of fever (usually defined as a single oral temperature ≥38.3°C or a sustained temperature ≥38.0°C over 1 hour) in a patient with neutropenia.

typically occurs to patients undergoing chemotherapy or other bone marrow supression tx

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21
Q

Symptoms of neutropenic sepsis

A

-chills
-malaise
- weakness
- signs of systemic infection, such as tachycardia, hypotension, or altered mental status.

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22
Q

Pathogens which typically affect patients with neutropaenic sepsis

A

-Pseudomonas aeruginosa,
Candida species, Aspergillus species, Staphylococcus Aeurus,
Enterococcus species
Escherichia coli
Streptococcus pneumoniae
Herpes Simplex Virus

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23
Q

managment of neutropaenic sepsis

A

-Sepsis 6
- consider anti-fungals and and antivirals
granulocyte colony-stimulating factors (G-CSF) to stimulate neutrophil production
-Consultation with Hematology/Oncology Specialists

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24
Q

Shock

A

Shock is a life-threatening medical emergency characterized by inadequate tissue perfusion, resulting in cellular hypoxia and organ dysfunction.

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25
what are the types of shock
-Hypovolemic shock -Cardiogenic Shock -Distributive Shock -Obstructive Shock
26
Further breakdown of distributive shock
- anaphylactic shock -neutrogenic shock - septic shock
27
Managment of shock
- ABCDE response - fluid resus -vasopressors -O2 managment - underlying causes
28
Neutropathic pain
Neuropathic pain may be defined as pain which arises following damage or disruption of the nervous system. It is often difficult to treat and responds poorly to standard analgesi
29
Examples of neutropathic pain
- diabetic neuropathy - post-herpetic neuralgia -trigeminal neuralgia -prolapsed intervertebral disc
30
First line treatment of neuropathic pain?
first-line treatment*: amitriptyline, duloxetine, gabapentin or pregabalin
31
What if the first-line treatment when neuropain is not manage the pain?
Try the other three drugs - amitriptyline, duloxetine, gabapentin or pregabline Drugs should be switched, not added
32
Rescue therapy Drug for neuropathic pain
Tramadol
33
When is Capsaicin used?
Localised neuropathic pain (e.g post-herpes)
34
Opioids
Opioids include substances like endorphins, semi-synthetic, and synthetic compounds that act on opioid receptors
35
G-coupled receptors for opioids
These receptors, present in the CNS, mediate the actions of opioids.
36
Mu (µ) Receptors:
* Brain, brainstem, and spinal cord. * **µ1-receptors**: Involved in **pain transmission; activation leads to analgesia** * **µ2- and µ3-receptors**: Found in the brainstem; their **activation causes** * respiratory depression * reduced gastrointestinal motility, * vasodilation * pupillary constriction in overdose.
37
Kappa (κ) Receptors:
Spread throughout the brain, brainstem, and spinal cord. Associated with cognitive effects, dysphoria, hallucinations, and depressed consciousness.
38
Delta (δ) Receptors:
Almost exclusively in the brain and brainstem. Potentiate µ-receptors, enhancing analgesia, respiratory depression, and dependence.
39
Endogenous Opioids
Include endorphins, dynorphins, and enkephalins, produced mainly in the brain and brainstem. β-Endorphin: Targets µ-receptors, influences appetite, sexual behaviour, and pain control during exercise. Met-enkephalin: Acts on δ-receptors, modulating the flight-or-fight response. Dynorphin: Involved in appetite, mood, and stress regulation.
40
Which enzyme system is responsible for opioid metabolism?
cytochrome P450 (CYP450
41
Phase I metabolism of opioids
* ***oxidation, reduction, and hydrolysis*** Cytochrome P450 enzymes ***CYP3A4 and CYP2D6*** —> modifying opioids to form more water-soluble metabolites. Example: **Codeine —>CYP2D6 —>morphine** (more active)
42
Phase II of opioid metabolism
Involves conjugation reactions like glucuronidation. Morphine is glucuronidated to morphine-3-glucuronide (inactive) and morphine-6-glucuronide (active and potent).
43
Genetic variability of opioid breakdown
Genetic polymorphisms in CYP450 enzymes, especially CYP2D6, can significantly affect the metabolism of certain opioids (like codeine and tramadol), leading to variability in clinical response.
44
Active metabolites of opioid breakdown
Some opioids have active metabolites that contribute to their analgesic effect or side effects. For example, the metabolites of morphine include both analgesic and neuroexcitatory compounds.
45
Renal excretion of opioids
Most opioid metabolites are excreted by the kidneys. Renal impairment can lead to the accumulation of these metabolites, increasing the risk of toxicity, especially in opioids with active metabolites.
46
Palliative care prescribing
offer patients with advanced and progressive disease regular oral modified-release (MR) or oral immediate-release morphine (depending on patient preference), with oral immediate-release morphine for breakthrough pain No co-morbidities, use 20-30mg of MR with 5mg morphine for breakthrough pain I.e 15mg modified-release morphine tablets twice a day with 5mg of oral morphine solution as required
47
Side effects of morphine and side prescriptions
-constipation (laxatives) - nausea and vomiting (antiemetic) - respiratory depression - drowsiness (adjust prescription if an issue) Oral morphine is preferred to transdermal morphine prescription
48
Breakthrough dose calculation
- Breakthrough dose morphine is 1/6 of daily dose - all patients who receive opioid should be given a laxative - care should be taken with patients with chronic kidney disease
49
Palliative care and renal impairment prescriptions
oxycodone is preferred to morphine in palliative patients with mild-moderate renal impairment if renal impairment is more severe, alfentanil, buprenorphine and fentanyl are preferred
50
Metastatic bone pain prescription
may respond to strong opioids, bisphosphonates or radiotherapy. Studies do not support use of NSAIDS Strong opioids have the lowest number needed to treat for relieving the pain and can provide quick relief, in contrast to radiotherapy and bisphosphonates*. All patients, however, should be considered for referral to a clinical oncologist for consideration of further treatments such as radiotherapy
51
How to increase opioid doses
Dose should be increased by 30-50% Add bisphosphonates, radiotherapy and denosumab to treat metastatic bone pain.
52
Transient side effects of opioids
Nausea Drowsiness
53
Persistent side effects of opioids
Constipation
54
Conversion between opioids
* Oral codeine to oral morphine- divide by 10 * Oral tramadol to oral morphine - divide by 10
55
Morphine to oxycodone conversion
Divide by 1.5 or 2
56
Oral morphine to subcutaneous morphine conversion
Divide by 2
57
Oral morphine to subcutaneous diamorphine
Divide by 3
58
Oral oxycodone to subcutaneous diamorphine
Divide by 1.5
59
Diagnostic criteria for AKI
Rise in creatinine of 26µmol/L or more in 48 hours OR >= 50% rise in creatinine over 7 days OR Fall in urine output to < 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) OR >= 25% fall in eGFR in children / young adults in 7 days.
60
Stage 1 AKI criteria
Increase in creatinine to 1.5-1.9 times baseline, or Increase in creatinine by ≥26.5 µmol/L, or Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
61
Stage 2 AKI criteria
Increase in creatinine to 2.0 to 2.9 times baseline, or Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
62
Stage 3 AKI criteria
* Increase in creatinine to ≥ 3.0 times baseline, or * Increase in creatinine to ≥353.6 µmol/L or * Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or * The initiation of kidney replacement therapy, or, * In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2
63
When to refer to a nephrologist with AKIs
Renal tranplant ITU patient with unknown cause of AKI Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma AKI with no known cause Inadequate response to treatment Complications of AKI Stage 3 AKI (see guideline for details) CKD stage 4 or 5 Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
64
What increases the risk of AKIs
Emergency surgery, ie, risk of sepsis or hypovolaemia Intraperitoneal surgery CKD, ie if eGFR < 60 Diabetes Heart failure Age >65 years Liver disease Use of nephrotoxic drugs NSAIDs aminoglycosides ACE inhibitors/angiotensin II receptor antagonists diuretics
65
Acute interstitial nephritis
Accounts to 25% of drug-induced AKis
66
Causes of AIN
drugs: the most common cause, particularly antibiotics penicillin rifampicin NSAIDs allopurinol furosemide systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome infection: Hanta virus , staphylococci
67
Pathophysiology of AIN
histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules
68
Features of AIN
fever, rash, arthralgia eosinophilia mild renal impairment hypertension
69
Investigations for AIN
sterile pyuria white cell casts
70
Anterpartum haemorrhage
Antepartum haemorrhage is defined as bleeding from the genital tract after 24 weeks pregnancy, prior to delivery of the fetus
71
Placental abruption
shock out of keeping with visible loss pain constant tender, tense uterus* normal lie and presentation fetal heart: absent/distressed coagulation problems beware pre-eclampsia, DIC, anuria
72
Placental praevia
shock in proportion to visible loss no pain uterus not tender lie and presentation may be abnormal fetal heart usually normal coagulation problems rare small bleeds before large vaginal examination should not be performed in primary care for suspected antepartum haemorrhage - women with placenta praevia may haemorrhage
73
Threatened miscarriage
painless vaginal bleeding occurring before 24 weeks, but typically occurs at 6 - 9 weeks the bleeding is often less than menstruation cervical os is closed complicates up to 25% of all pregnancies
74
Missed (delayed) miscarriage
a gestational sac which contains a dead fetus before 20 weeks without the symptoms of expulsion mother may have light vaginal bleeding / discharge and the symptoms of pregnancy which disappear. Pain is not usually a feature cervical os is closed when the gestational sac is > 25 mm and no embryonic/fetal part can be seen it is sometimes described as a 'blighted ovum' or 'anembryonic pregnancy'
75
Inevitable miscarriage
- heavy bleeding with clots and pain Cervical os is open
76
Incom plete miscarriage
not all products of conception have been expelled pain and vaginal bleeding cervical os is open
77
Expectant management of miscarriage
Waiting for a spontaneous miscarriage' First-line and involves waiting for 7-14 days for the miscarriage to complete spontaneously If expectant management is unsuccessful then medical or surgical management may be offered
78
Medical or surgical management.of miscarriage risks
increased risk of haemorrhage she is in the late first trimester if she has coagulopathies or is unable to have a blood transfusion previous adverse and/or traumatic experience associated with pregnancy (for example, stillbirth, miscarriage or antepartum haemorrhage) evidence of infection
79
Medical management of missed miscarriage
oral mifepristone. 48 hours later, misoprostol If bleeding has not started within 48 hours after misoprostol treatment, they should contact their healthcare professional
80
Incomplete miscarriage management
a single dose of misoprostol (vaginal, oral or sublingual)
81
Management of all miscarriages
women should be offered antiemetics and pain relief a pregnancy test should be performed at 3 weeks
82
Surgical management of miscarriage
Undergoing a surgical procedure under local or general anaesthetic' The two main options are vacuum aspiration (suction curettage) or surgical management in theatre Vacuum aspiration is done under local anaesthetic as an outpatient
83
Causes of recurrent miscarriages
antiphospholipid syndrome endocrine disorders: poorly controlled diabetes mellitus/thyroid disorders. Polycystic ovarian syndrome uterine abnormality: e.g. uterine septum parental chromosomal abnormalities smoking
84
Immediate first aid for burns
airway, breathing, circulation burns caused by heat: remove the person from the source. Within 20 minutes of the injury irrigate the burn with cool (not iced) water for between 10 and 30 minutes. Cover the burn using cling film, layered, rather than wrapped around a limb electrical burns: switch off power supply, remove the person from the source chemical burns: brush any powder off then irrigate with water. Attempts to neutralise the chemical are not recommended
85
Wallace’s rule of nines
head + neck = 9%, each arm = 9%, each anterior part of leg = 9%, each posterior part of leg = 9%, anterior chest = 9%, posterior chest = 9%, Anterior abdomen = 9%, posterior abdomen = 9% The palmar surface is approximately 1%
86
Superficial epidermal burn
First degree Red and painful, no dry blisters
87
Patial thickness (superficial dermal)
Second degree burn Pale piping, painful, blistered and reduced cap refill time
88
Partial thickness burn (deep dermal)
Second degree Typically white, but may have non-blanching erythema Reduced sensation Painful to deep pressure
89
Full thickness burn
- third degree burn - white (waxy) - brown (leathery) Black in colour with no blisters or pain
90
Acynotic congenital heart disease
ventricular septal defects (VSD) - most common, accounts for 30% atrial septal defect (ASD) patent ductus arteriosus (PDA) coarctation of the aorta aortic valve stenosis
91
Cyanotic causes of congenital heart disease
tetralogy of Fallot transposition of the great arteries (TGA) tricuspid atresia
92
Peripheral cyanosis in neonatal period
very common in the first 24 hours of life and may occur when the child is crying or unwell from any cause
93
Central cyanosis in neonatal period
Central cyanosis can be recognised clinically when the concentration of reduced haemoglobin in the blood exceeds 5g/dl
94
Nitrogen washout test
nitrogen washout test (also known as the hyperoxia test) may be used to differentiate cardiac from non-cardiac causes. The infant is given 100% oxygen for ten minutes after which arterial blood gases are taken. A pO2 of less than 15 kPa indicates cyanotic congenital heart disease
95
Management of suspected cyanotic congenital heart disease
supportive care prostaglandin E1 e.g. alprostadil used to maintain a patent ductus arteriosus in ductal-dependent congenital heart defect this can act as a holding measure until a definite diagnosis is made and surgical correction performed
96
Acrocyanosis
refers to cyanosis around the mouth and the extremities such as the hands and feet occurs immediately after birth in healthy infants. It is a common finding and may persist for 24 to 48 hours.
97
Teraology of Fallot
Most common cause of congenital heart disease Presents around 1-2 months but may not be picked up until the baby is 6 months old
98
Four characteristic features of teralogy of fallot
ventricular septal defect (VSD) right ventricular hypertrophy right ventricular outflow tract obstruction, pulmonary stenosis overriding aorta severity of the right ventricular outflow tract obstruction determines the degree of cyanosis and clinical severity
99
Features of TOF
cyanosis unrepaired TOF infants may develop episodic hypercyanotic 'tet' spells due to near occlusion of the right ventricular outflow tract features of tet spells include tachypnoea and severe cyanosis that may occasionally result in loss of consciousness they typically occur when an infant is upset, is in pain or has a fever causes a right-to-left shunt ejection systolic murmur due to pulmonary stenosis (the VSD doesn't usually cause a murmur) a right-sided aortic arch is seen in 25% of patients chest x-ray shows a 'boot-shaped' heart, ECG shows right ventricular hypertrophy
100
Management of TOF
surgical repair is often undertaken in two parts cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm
101
Transposition of the great arteries (TGA)
Transposition of the great arteries (TGA) is a form of cyanotic congenital heart disease. It is caused by the failure of the aorticopulmonary septum to spiral during septation. Children of diabetic mothers are at an increased risk of TGA.
102
Anatomical changes in TGA
aorta leaves the right ventricle pulmonary trunk leaves the left ventricle
103
Clinical features of TGA
cyanosis tachypnoea loud single S2 prominent right ventricular impulse 'egg-on-side' appearance on chest x-ray
104
Management of TGA
maintenance of the ductus arteriosus with prostaglandins surgical correction is the definite treatment.
105
Extramural haematoma
collection of blood that is between the skull and the dura. It is almost always caused by trauma and most typically by ˜low-impact' trauma (e.g. a blow to the head or a fall). Collection is typically in the temporal region (MIDDLE MENINGEAL ARTERY)
106
patient who initially loses, briefly regains and then loses again consciousness after a low-impact head injury.
Extradural haematoma Ludic period
107
Imaging of extradural haematoma
biconvex (or lentiform), hyperdense collection around the surface of the brain. They are limited by the suture lines of the skull.
108
Treatment of extradural haematoma
treatment is craniotomy and evacuation of the haematoma.
109
Hypoglycaemia causes
insulinoma - increased ratio of proinsulin to insulin self-administration of insulin/sulphonylureas liver failure Addison's disease alcohol causes exaggerated insulin secretion mechanism is thought to be due to the effect of alcohol on the pancreatic microcirculation → redistribution of pancreatic blood flow from the exocrine into the endocrine parts → increased insulin secretion nesidioblastosis - beta cell hyperplasia
110
Features of hypoglycaemia
blood glucose levels and the severity of symptoms are not always correlated, especially in patients with diabetes. blood glucose concentrations <3.3 mmol/L cause autonomic symptoms due to the release of glucagon and adrenaline (average frequency in brackets): Sweating Shaking Hunger Anxiety Nausea blood glucose concentrations below <2.8 mmol/L cause neuroglycopenic symptoms due to inadequate glucose supply to the brain: Weakness Vision changes Confusion Dizziness Severe and uncommon features of hypoglycaemia include: Convulsion Coma
111
Management of hypoglycaemia in hospital settings
If the patient is alert, a quick-acting carbohydrate may be given (as above) If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given. Alternatively, intravenous 20% glucose solution may be given through a large vein
112
Managment of hypoglycaemia
in the community (for example, diabetes mellitus patients who inject insulin): Initially, oral glucose 10-20g should be given in liquid, gel or tablet form Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel. A 'HypoKit' may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
113
Subarachnoid haemorrhage (SAH)
intracranial haemorrhage that is defined as the presence of blood within the subarachnoid space, i.e. deep to the subarachnoid layer of the meninges.
114
Causes of spontaneous SAH
intracranial aneurysm (saccular ˜berry' aneurysms) accounts for around 85% of cases conditions associated with berry aneurysms include hypertension,adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta arteriovenous malformation pituitary apoplexy mycotic (infective) aneurysms
115
Classical presentation of SAH
- Headache (sudden onset, thunderclap) - severe (worst in my life) - occipital typically peaking in intensity within 1 to 5 minutes there may be a history of a less-severe 'sentinel' headache in the weeks prior to presentation nausea and vomiting meningism (photophobia, neck stiffness) coma seizures ECG changes including ST elevation may be seen this may be secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines
116
Investigation for SAH
Non-contrast CT (acute blood, hypodense, bright on CT) If CT done within 6 hours of symptoms, may appear to be normal LP after 12 hours of symptoms shows Xathochromia CSF will also show normal or raised opening pressure
117
Managment of SAH
supportive bed rest analgesia venous thromboembolism prophylaxis discontinuation of antithrombotics (reversal of anticoagulation if present) vasospasm is prevented using a course of oral nimodipine intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
118
Complications of SAH
re-bleeding happens in around 10% of cases and most common in the first 12 hours if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged associated with a high mortality (up to 70%) hydrocephalus hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset ensure euvolaemia (normal blood volume) consider treatment with a vasopressor if symptoms persist hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH)) seizures
119
Predictive factors of SAH
conscious level on admission age amount of blood visible on CT head
120
What is subdural haematoma
subdural haematoma is a collection of blood deep to the dural layer of the meninges. The blood is not within the substance of the brain and is therefore called an ˜extra-axial' or ˜extrinsic' lesion. They can be unilateral or bilateral.
121
Classifications of subdural haemorrhage
Acute: Symptoms usually develop within 48 hours of injury, characterised by rapid neurological deterioration Subacute: Symptoms manifest within days to weeks post-injury, with a more gradual progression. Chronic: Common in the elderly, developing over weeks to months. Patients may not recall a specific head injury.
122
Neurological features of subdural haemorrhage
Altered Mental Status: Ranging from mild confusion to deep coma. Fluctuations in the level of consciousness are common. Focal Neurological Deficits: Weakness on one side of the body, aphasia, or visual field defects, depending on the haematoma's location. Headache: Often localised to one side, worsening over time. Seizures: May occur, particularly in acute or expanding hematomas.
123
Physical examination findings of subdural haemorrhage
Papilloedema: Indicates raised intracranial pressure. Pupil Changes: Unilateral dilated pupil, especially on the side of the haematoma, indicating compression of the third cranial nerve. Gait Abnormalities: Including ataxia or weakness in one leg. Hemiparesis or Hemiplegia: Reflecting the mass effect and midline shift.
124
Behavioural and cognitive change in subdural haemorrhage
Memory loss- especially in chronic SDH Personality Changes: Irritability, apathy, or depression. Cognitive Impairment: Difficulty with attention, problem-solving, and other executive functions.
125
Other associated features of SDH
Nausea and Vomiting: Secondary to increased intracranial pressure. Drowsiness: Progressing to stupor and coma in severe cases. Signs of Increased Intracranial Pressure: Such as bradycardia, hypertension, and respiratory irregularities (Cushing's triad).
126
GCS
Motor, verbal and eye features (M6, V5, E4)
127
Motor response
6. Infant moves spontaneously or purposefully 5. Infant withdraws from touch 4. Infant withdraws from pain 3. Abnormal flexion to pain for an infant (decorticate response) 2. Extension to pain (decerebrate response) 1. No motor response
128
Verbal response
5. Orientated 4. Confused 3. Words 2. Sounds 1. None
129
Eye response
4. Spontaneous 3. To speech 2. To pain 1. None
130
Fluid therapy in adults
25-30 ml/kg/ day 1 mol/kg/day of K+, Na+ and CL- Approximately 50-100g per day of glucose to limit strvation and ketosis
131
Prescription of fluids contradictions and concerns
0.9% saline if large volumes are used there is an increased risk of hyperchloraemic metabolic acidosis Hartmann's contains potassium and therefore should not be used in patients with hyperkalaemia
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Fluid therapy in children (when required)
IV fluids required when: the child is > 10% dehydrated, or the child is if 5-10% dehydrated and oral or enteral rehydration is not tolerated or possible.
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24hr fluid requirement- under 10kg
100ml/kg
134
24hr fluid requirement 10-20kg
100 mL/kg for the first 10 kg 50 mL/kg for each 1 kg body weight over 10 kg
135
24 hr fluid requirement over 20kg
100 mL/kg for the first 10 kg 50 mL/kg for each 1 kg body weight between 10-20 kg 20 mL/kg for each 1 kg body weight over 20 kg (max. 2 litres in females, 2.5 litres in males)
136
IV fluids in children
The fluid type routinely used is 0.9% sodium chloride + 5% dextrose. Potassium is added as required.
137
Hyperosmolar hyperglycaemic state (HHS)
Medical emergency with 20% mortality Hyperglycaemia results in osmotic diuresis, severe dehydration, and electrolyte deficiencies. HHS typically presents in the elderly with type 2 diabetes mellitus (T2DM).
138
Pathophysiology of HHS
Hyperglycaemia results in osmotic diuresis, severe dehydration, and electrolyte deficiencies. HHS typically presents in the elderly with type 2 diabetes mellitus (T2DM).
139
Precipitating factors of HHS
- intercurrent illness -dementia -sedative drugs
140
Clinical features of HHS
- occurs over many days, associated with dehydration and metabolic disturbances - volume loft (polyuria, polydipsia, signs of dehydration) Systemic - lethargy - nausea and vomiting neurological -altered level of consciousness -focal neurological deficits haematological -hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
141
Signs and symptoms of HHS
hypovolaemia marked hyperglycaemia (>30 mmol/L) significantly raised serum osmolarity (> 320 mosmol/kg) can be calculated by: 2 * Na+ + glucose + urea no significant hyperketonaemia (<3 mmol/L) no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 - acidosis can occur due to lactic acidosis or renal impairment)
142
Managment of HHS
fluid replacement fluid losses in HHS are estimated to be between 100 - 220 ml/kg IV 0.9% sodium chloride solution typically given at 0.5 - 1 L/hour depending on clinical assessment potassium levels should be monitored and added to fluids depending on the level insulin should not be given unless blood glucose stops falling while giving IV fluids venous thromboembolism prophylaxis patients are at risk of thrombosis due to hyperviscosity
143
Complications of HHS
Vascular complications: - MI - stroke
144
What are the causes of hypercalcaemia?
1. Primary hyperparathyroidism 2. Malignancy (SCLS, bone mets, myeloma) 3. Sarcoidosis 4. Vit D intoxication 5. Acromegaly 6. Thyrotoxicosis 7. Milk- alkali syndrome 8. Thiazides 9/ calcium containing antacids 10 dehydatraion 11 Addison’s disease 12 pager’s disease of the bone
145
Features of hypercalcaemia
bones, stones, groans and psychic moans' corneal calcification shortened QT interval on ECG hypertension
146
Hyperkalaemia
- regulated by a number of factors including aldosterone, acid-base balance and insulin levels - metabolic acidosis is associated
147
Causes of hyperkalaemia
acute kidney injury drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin** metabolic acidosis Addison's disease rhabdomyolysis massive blood transfusion - salt substitutes - bananas, oranges, kiwi, avos, spinach and tonatoes
148
Managment of hyperkalaemia
- Stabilisation of the cardiac membrane IV calcium gluconate does NOT lower serum potassium levels Short-term shift in potassium from extracellular (ECF) to intracellular fluid (ICF) compartment combined insulin/dextrose infusion nebulised salbutamol Removal of potassium from the body calcium resonium (orally or enema) enemas are more effective than oral as potassium is secreted by the rectum loop diuretics dialysis haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia
149
Staging of hyperkalaemia
mild: 5.5 - 5.9 mmol/L moderate: 6.0 - 6.4 mmol/L severe: ≥ 6.5 mmol/L
150
ECG changes of hyperkalaemia
peaked or 'tall-tented' T waves (occurs first) loss of P waves broad QRS complexes sinusoidal wave pattern
151
Practical managment of hyperkalaemia
IV calcium gluconate: to stabilise the myocardium insulin/dextrose infusion: short-term shift in potassium from ECF to ICF other treatments such as nebulised salbutamol may be given to temporarily lower the serum potassium Further management stop exacerbating drugs e.g. ACE inhibitors treat any underlying cause lower total body potassium calcium resonium loop diuretics dialysis
152
Hypernatraemia causes
- dehydration -osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma diabetes insipidus excess IV saline
153
Risks of treating hypernatremia
owering of other osmolytes (and importantly water) occurs at a slower rate, predisposing to cerebral oedema, resulting in seizures, coma and death Should be corrected at 0.5mmol/hour
154
Causes of hypocalcaemia
vitamin D deficiency (osteomalacia) chronic kidney disease hypoparathyroidism (e.g. post thyroid/parathyroid surgery) pseudohypoparathyroidism (target cells insensitive to PTH) rhabdomyolysis (initial stages) magnesium deficiency (due to end organ PTH resistance) massive blood transfusion acute pancreatitis
155
False positive hypocalcaemia
Contamination of blood samples with EDTA may also give falsely low calcium levels.
156
Managment of hypocalcaemia
severe hypocalcaemia (e.g. carpopedal spasm, tetany, seizures or prolonged QT interval) requires IV calcium replacement the preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes intravenous calcium chloride is more likely to cause local irritation ECG monitoring is recommended further management depends on the underlying cause
157
Causes of Hypomagnesaemia
drugs diuretics proton pump inhibitors total parenteral nutrition diarrhoea may occur with acute or chronic diarrhoea alcohol hypokalaemia hypercalcaemia e.g. secondary to hyperparathyroidism calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle metabolic disorders Gitleman's and Bartter's
158
Features of hypomagnesaemia
paraesthesia tetany seizures arrhythmias decreased PTH secretion → hypocalcaemia ECG features similar to those of hypokalaemia exacerbates digoxin toxicity
159
Treatment of hypoganesaemia (<0.4mmol/L or tetany, arrhythmias or seizures)
intravenous magnesium replacement is commonly given. an example regime would be 40 mmol of magnesium sulphate over 24 hours
160
>0.4 mol/L hypomagnesaeima managment
oral magnesium salts (10-20 mmol orally per day in divided doses) diarrhoea can occur with oral magnesium salts
161
Pseudohyponatremia causes
Hyperlipiddaemia Taking blood from a drip arm
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Urinary sodium > 20 mmol/l
Sodium depletion, renal loss (patient often hypovolaemic) diuretics: thiazides, loop diuretics Addison's disease diuretic stage of renal failure Patient often euvolaemic SIADH (urine osmolality > 500 mmol/kg) hypothyroidism
163
Urinary sodium < 20 mmol/l
Sodium depletion, extra-renal loss diarrhoea, vomiting, sweating burns, adenoma of rectum Water excess (patient often hypervolaemic and oedematous) secondary hyperaldosteronism: heart failure, liver cirrhosis nephrotic syndrome IV dextrose psychogenic polydipsia
164
Atrial fibrillation
Symptomatic palpitations and inefficient cardiac function probably the most important aspect of managing patients with AF is reducing the increased risk of stroke which is present in these patients.
165
Types of atrial fibrillation
- paroxysmal AF- episodes of AF terminate spontaneously. Such episodes last less than 7 days - Persistent AF- non self-terminating AF - permanent AF- continuous atrial fibrillation can’t be cardioverted or deemed inappropriate
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Symptoms of AF
palpitations dyspnoea chest pain
167
Signs of AF
Irregular irregular puls
168
Investigations of AF
- ECG
169
Management of AF
- rate and rhythm control - reducing stroke risk
170
Rate vs rhythm control
rate control **bold text control Rate ** : accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function rhythm control: try to get the patient back into, and maintain, normal sinus rhythm. This is termed cardioversion. Drugs (pharmacological cardioversion) and synchronised DC electrical shocks (electrical cardioversion) may be used for this purpose
171
What drugs are used for rate control?
Any of the following 2 a betablocker diltiazem digoxin
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CHA2DS2VS score elements
C- congenital H- hypertension (or treated) A2- age D- diabetes S2- prior stroke, TIA or thromboembolism V- vascular disease (including ischameic heart disease, peripheral artery disease S- sex (female)
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CHA2DS2-VASc score distribution
C- 1 H-1 A >75 (2 points) A 65-74 (1 points) D (1 points) S2- (2 points) V (1 points) S (1 points)
174
What to do with the CHADVASC score?
0 - no treatment needed 1- males consider anticoagulant, females don’t need 2- offer anticoagulants
175
HASBLED score vs ORBIT score
Orbit score is encouraged to be used by NICE rather than HASBLED score
176
ORBIT score
0-2, low risk which is 2.4 bleeds per 100 pt per year 3, medium, 4.7 4-7, high, 8.1
177
HASBLED score
Haemoglobin ‘ Age >74 Bleeding (GI bleed, intracranial bleed, haemorrhagic stroke) Renal impairment (GFR <60 ml/min) Treatment with antiplatelet agent
178
Points in HAS-BLED
H-2 A-1 S B- 2 L E- 1 D- 1
179
Doacs to reduce AF stroke risk
apixaban dabigatran edoxaban Warfarin is recommended as second line if DOAC contradicted Do not prescribe aspirin
180
When cardioversion in AF
electrical cardioversion as an emergency if the patient is haemodynamically unstable electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred.
181
How ECG and electrocardioversion carried out in AF
Electrical cardioversion is synchronised to the R wave to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced.
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AF onset <48 hours
If AF less than 48 hours, patient should be heparanised Patients with risk of ischaemic stroke should be put on lifelong oral anticoagulation Otherwise cardiovert the patient
183
Cardioversion in AF patients onset <48 hours
electrical - 'DC cardioversion' pharmacology - amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease
184
Onset > 48 hours of AF
AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion. An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately.
185
What if there is high risk of AF failure in onset >48 hours
If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion
186
Following electrocardioversion in AF patients
- anticoagulants the patient for at least 4 weeks
187
Features of AF
AF may present with palpitations, dyspnoea, dizziness/syncope many cases are asymptomatic and are found as an incidental finding the pulse is irregularly irregular
188
Diagnosis of AF
ECG: absent P waves a 24 hour ECG or event recorder is useful where paroxysmal atrial fibrillation is suspected echocardiography is not required in all cases
189
What are the two key elements of managing AF
1. reducing the risk of stroke 2. controlling the heart rate
190
Agents used for effective pharmacological cardioversion
-amiodarone -flecainide (if no structural heart disease) -others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone
191
Less effective agents for pharmacological cardioversion
beta-blockers (including sotalol) calcium channel blockers digoxin disopyramide procainamide
192
Management of stroke
F ollowing a stroke or TIA it is obviously important to exclude a haemorrhage before starting any anticoagulation or antiplatelet therapy for longer-term stroke prevention, NICE Clinical Knowledge Summaries recommend warfarin or a direct thrombin or factor Xa inhibitor the timing of when to start depends on whether it is a TIA or stroke following a TIA, anticoagulation for AF should start immediately once imaging has excluded haemorrhage in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. Antiplatelet therapy should be given in the intervening period. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed
193
Atrial flutter
- sawtooth appearance - rate often 300/ min - ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min - flutter waves will be visible following carotid sinus massage or adenosine
194
Management of Atrial flutter
is similar to that of atrial fibrillation although medication may be less effective atrial flutter is more sensitive to cardioversion however so lower energy levels may be used radiofrequency ablation of the tricuspid valve isthmus is curative for most patients
195
Broad complex tactic
AV dissociation fusion or capture beats positive QRS concordance in chest leads marked left axis deviation history of IHD lack of response to adenosine or carotid sinus massage QRS > 160 ms
196
Peri-arrest: bradycardia
1. identifying the presence of signs indicating haemodynamic compromise - 'adverse signs' 2. identifying the potential risk of asystole
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Adverse signs of bradycardia
shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness syncope myocardial ischaemia heart failure
198
What is the first line treatment of bradycardia (adverse signs have been observed)
Atropine (500mg IV)
199
What to do if unsatisfactory response to first line intervention of bradycardia
atropine, up to a maximum of 3mg transcutaneous pacing isoprenaline/adrenaline infusion titrated to response If no response, get help with transvenous pacing
200
Risk factors for asystole
complete heart block with broad complex QRS recent asystole Mobitz type II AV block ventricular pause > 3 seconds
201
Peri-arrest tachycardia adverse signs
shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness syncope myocardial ischaemia heart failure
202
Management of tachcardia:
adverse signs are present then synchronised DC shocks should be given. Up to three shocks can be given, then seek expert help after this
203
Broad- complex tachycardia
assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block) loading dose of amiodarone followed by 24 hour infusion
204
Irregular Broad- complex tachycardia
seek expert help. Possibilities include: atrial fibrillation with bundle branch block - the most likely cause in a stable patient atrial fibrillation with ventricular pre-excitation torsade de pointes
205
Regular narrow-complex tachycardia
vagal manoeuvres followed by IV adenosine if the above is unsuccessful consider a diagnosis of atrial flutter and control rate (e.g. beta-blocker
206
Irregular narrow complex tachycardia
probable atrial fibrillation if onset < 48 hr consider electrical or chemical cardioversion rate control: beta-blockers are usually first-line unless there is a contraindication
207
Torsades de pointes
- twisting of the points -forms of polymorphic ventricular tachycardia associated with long QT syndrome - can cause VF - can lead to sudden death
208
Causes of Long QT-syndrome
congenital Jervell-Lange-Nielsen syndrome Romano-Ward syndrome antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants antipsychotics chloroquine terfenadine erythromycin electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia myocarditis hypothermia subarachnoid haemorrhage
209
What is the management of Torsades de pointes?
IV magnesium sulphate
210
Ventricular tachycardia
Ventricular tachycardia (VT) is broad-complex tachycardia originating from a ventricular ectopic focus. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.
211
What are the two main types of VT?
- monomorphic VT - Polymorphic VT
212
Causes of Monomorphic VT
most commonly caused by myocardial infarction
213
Polymorphic VT causes
subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval. The causes of a long QT interva
214
Congenital causes of prolonged QT interval
Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel) Romano-Ward syndrome (no deafness)
215
Drugs which cause long QT
amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, fluoxetine chloroquine terfenadine erythromycin
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“Other” causes of prolonged QT intercal
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia acute myocardial infarction myocarditis hypothermia subarachnoid haemorrhage
217
Management of VT
- if any adverse signs (systolic BP < 90 mmHg, chest pain, heart failure), then IMMEDIATE CARDIOVERSION -If absence of symptoms, then consider antiarrhythmics - if this fails, then SYNCHRONISED DC shock
218
Drug tx of VT
amiodarone: ideally administered through a central line lidocaine: use with caution in severe left ventricular impairment procainamide
219
Vermapil and VT
CONTRADICTED
220
What to do if drug therapy fails in VT
electrophysiological study (EPS) implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
221
Causes of metabolic acidosis
vomiting / aspiration (e.g. peptic ulcer leading to pyloric stenos, nasogastric suction) diuretics liquorice, carbenoxolone hypokalaemia primary hyperaldosteronism Cushing's syndrome Bartter's syndrome congenital adrenal hyperplasia LOSS OF H+ OR GAIN OR BICARD
222
Causes of respiratory acidosis
COPD decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema sedative drugs: benzodiazepines, opiate overdose
223
Causes of reps alkalosis
anxiety leading to hyperventilation pulmonary embolism salicylate poisoning CNS disorders: stroke, subarachnoid haemorrhage, encephalitis altitude pregnancy
224
Normal anion gap metabolic acidosis causes
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula renal tubular acidosis drugs: e.g. acetazolamide ammonium chloride injection Addison's disease
225
Rasied anion gap metabolic acidosis causes
lactate: shock, hypoxia ketones: diabetic ketoacidosis, alcohol urate: renal failure acid poisoning: salicylates, methanol
226
Anion gap calculation
(sodium + potassium) - (bicarbonate + chloride) A normal anion gap is 8-14 mmol/L
227
Causes of normal anion gap or hyperchloraemic metabolic acidosis (6)
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula renal tubular acidosis drugs: e.g. acetazolamide ammonium chloride injection Addison's disease
228
ROME
Respiratory = Opposite low pH + high PaCO2 i.e. acidosis, or high pH + low PaCO2 i.e. alkalosis Metabolic = Equal low pH + low bicarbonate i.e. acidosis, or high pH + high bicarbonate i.e. akalosis
229
Metabolic component of ABG
Metabolic component: What is the bicarbonate level/base excess? bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l) suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis) bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l) suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)
230
Metabolic acidosis secondary to high lactate subcategories
lactic acidosis type A: sepsis, shock, hypoxia, burns lactic acidosis type B: metformin
231
Mechanism of metabolic alkalosis
activation of renin-angiotensin II-aldosterone (RAA) system is a key factor aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels in hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality
232
Salicylate overdose ABG
Mixed respiratory alkalosis and metabolic acidosis
233
Hypomagnesaemia causes
drugs diuretics proton pump inhibitors total parenteral nutrition diarrhoea may occur with acute or chronic diarrhoea alcohol hypokalaemia hypercalcaemia e.g. secondary to hyperparathyroidism calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle metabolic disorders Gitleman's and Bartter's
234
Features of hypomagnesaemia
- similar to hypocalaemia paraesthesia tetany seizures arrhythmias decreased PTH secretion → hypocalcaemia ECG features similar to those of hypokalaemia exacerbates digoxin toxicity
235
Treatment of hypomagnesaemia (<0.4mmol/L)
<0.4 mmol/L or tetany, arrhythmias, or seizures intravenous magnesium replacement is commonly given. an example regime would be 40 mmol of magnesium sulphate over 24 hours
236
Treatment of >0.4 mol/L magnesium
oral magnesium salts (10-20 mmol orally per day in divided doses) diarrhoea can occur with oral magnesium salts
237
Epistaxis
Nose bleeds Split into anterior and posterior bleeds Kiesselbach’s plexus (anterior and visible bleed) Posterior node bleeds more common in elderly and higher risk of apritation and airway compromise
238
Causes of epistaxis
most cases of epistaxis tend to be benign and self-limiting. Exacerbation factors include: nose picking nose blowing trauma to the nose insertion of foreign bodies bleeding disorders immune thrombocytopenia Waldenstrom's macroglobulinaemia juvenile angiofibroma benign tumour that is highly vascularised seen in adolescent males cocaine use the nasal septum may look abraded or atrophied, inquire about drug use. This is because inhaled cocaine cocaine is a powerful vasoconstrictor and repeated use may result in obliteration of the septum. hereditary haemorrhagic telangiectasia granulomatosis with polyangiitis
239
First aid management of epistaxis
Asking the patient to sit with their torso forward and their mouth open avoid lying down unless they feel faint his decreases blood flow to the nasopharynx and allows the patient to spit out any blood in their mouth it also reduces the risk of aspirating blood Pinch the cartilaginous (soft) area of the nose firmly this should be done for at least 20 minutes also ask the patient to breathe through their mouth.
240
Epistaxis when first aid measurements are successful
consider using a topical antiseptic such as Naseptin (chlorhexidine and neomycin) to reduce crusting and the risk of vestibulitis cautions to this include patients that have peanut, soy or neomycin allergies Mupirocin is a viable alternative admission and follow up care may be considered in patients under if a comorbidity (e.g. coronary artery disease, or severe hypertension) is present, an underlying cause is suspected they are aged under 2 years (as underlying causes such as haemophilia or leukaemia are more likely in this age group) self-care advice involves reducing the risk of re-bleeding patients should be informed that blowing or picking the nose, heavy lifting, exercise, lying flat, drinking alcohol or hot drinks should be avoided
241
If bleeding does not stop after 10-15 minuted of continuous pressure
cautery should be used initially if the source of the bleed is visible and cautery is tolerated it is not so well-tolerated in younger children! ask the patient to blow their nose in order to remove any clots. Be wary that bleeding may resume. use a topical local anaesthetic spray (e.g. Co-phenylcaine) and wait 3-4 minutes for it to take effect identify the bleeding point and apply the silver nitrate stick for 3-10 seconds until it becomes grey-white. Avoid touching areas which do not require treatment, and only cauterise one side of the septum as there is a risk of perforation. dab the area clean with a cotton bud and apply Naseptin or Muciprocin packing may be used if cautery is not viable or the bleeding point cannot be visualised anaesthetise with topical local anaesthetic spray (e.g. Co-phenylcaine) and wait for 3-4 minutes pack the patient's nose while they are sitting with their head forward, following the manufacturer's instructions pressure on the cartilage around the nostril can cause cosmetic changes and this should be reviewed after inserting the pack. examine the patient's mouth and throat for any continuing bleeding, and consider packing the other nostril as this increases pressure on the septum and offending vessel. patients should be admitted to hospital for observation and review, and to ENT if available
242
When should patients be referred to ED with epistaxis
haemodynamically unstable or compromised should be admitted to the emergency department
243
What occurs at ED when patients presents with epistaxis?
control bleeding with first aid measures in the interim patients with a bleed from an unknown or posterior source (i.e. the bleeding site cannot be located on speculum, bleeding from both nostrils or profuse) should be admitted to hospital.
244
Epistaxis emergency treatment?
sphenopalatine ligation in theatre
245
Carbon monoxide poisoning
- CO positioning causes left shift of the oxygen dissociation curve Causes tissue hypoxia Every year there are approximately 50 deaths due to CO poisoning
246
Pathophysiology of CO poisoning
carbon monoxide binds readily to haemoglobin, forming carboxyhaemoglobin → reduced oxygen-carrying capacity in carbon monoxide poisoning the oxygen saturation of haemoglobin decreases leading to an early plateau in the oxygen dissociation curve
247
Features of CO poisoning?
headache: 90% of cases nausea and vomiting: 50% vertigo: 50% confusion: 30% subjective weakness: 20% severe toxicity: 'pink' skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death
248
Investigations of CO poisoning?
pulse oximetry may be falsely high due to similarities between oxyhaemoglobin and carboxyhaemoglobin therefore a venous or arterial blood gas should be taken typical carboxyhaemoglobin levels < 3% non-smokers < 10% smokers 10 - 30% symptomatic: headache, vomiting > 30% severe toxicity an ECG is a useful supplementary investgation to look for cardiac ischaemia
249
Management of CO poisoning?
- assess in ED -100% high flow 02 non-rebreather mask -Hyperbaric oxygen
250
Features of lead poisoning
abdominal pain peripheral neuropathy (mainly motor) neuropsychiatric features fatigue constipation blue lines on gum margin (only 20% of adult patients, very rare in children) Acute intermittent porphyria Defective ferrochelatase and ALA dehydrates function
251
Investigations of Lead poisoning
the blood lead level is usually used for diagnosis. Levels greater than 10 mcg/dl are considered significant full blood count: microcytic anaemia. Blood film shows red cell abnormalities including basophilic stippling and clover-leaf morphology raised serum and urine levels of delta aminolaevulinic acid may be seen making it sometimes difficult to differentiate from acute intermittent porphyria urinary coproporphyrin is also increased (urinary porphobilinogen and uroporphyrin levels are normal to slightly increased) in children, lead can accumulate in the metaphysis of the bones although x-rays are not part of the standard work-up
252
Management of lead poisoning
various chelating agents are currently used: dimercaptosuccinic acid (DMSA) D-penicillamine EDTA dimercaprol
253
Organophosphate insecticide poisoning
inhibition of acetylcholinesterase leading to upregulation of nicotinic and muscarinic cholinergic neurotransmission. In warfare, sarin gas is a highly toxic synthetic organophosphorus compound that has similar effects.
254
Features of organophosphate insecticide poisoning SLUD
accumulation of acetylcholine (mnemonic = SLUD) Salivation Lacrimation Urination Defecation/diarrhoea cardiovascular: hypotension, bradycardia also: small pupils, muscle fasciculation
255
Management of Organophosphate insecticide poisoning
atropine the role of pralidoxime is still unclear - meta-analyses to date have failed to show any clear benefit
256
Paracetamol overdose
activated charcoal if ingested < 1 hour ago N-acetylcysteine (NAC) liver transplantation
257
Salicylate management
urinary alkalinization with IV bicarbonate haemodialysis
258
Opioid overdose
Naloxone
259
Benzodiazepines overdose
Flumazenil The majority of overdoses are managed with supportive care only due to the risk of seizures with flumazenil. It is generally only used with severe or iatrogenic overdoses.
260
Tricyclic antidepressant management
IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity arrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias dialysis is ineffective in removing tricyclics
261
Lithium management
mild-moderate toxicity may respond to volume resuscitation with normal saline haemodialysis may be needed in severe toxicity sodium bicarbonate is sometimes used but there is limited evidence to support this. By increasing the alkalinity of the urine it promotes lithium excretion
262
Warfarin management
Vitamin K, prothrombin complex
263
Heparin management
Vitamin K Prothrombin complex
264
Beta blocker overdose
if bradycardic then atropine in resistant cases glucagon may be used
265
Ethylene glycol overdose
fomepizole Can use ethanol as well
266
Methanol poisoning
fomepizole or ethanol haemodialysis
267
Digoxin overdose management
Digoxin-specific antibody fragments
268
Iron overdose management
Desferrioxamine, a chelating agent
269
Lead overdose
Dimercaprol, calcium edentate
270
Cyanide overdose management
Hydroxocobalamin; also combination of amyl nitrite, sodium nitrite, and sodium thiosulfate
271
Synthetic cannaboid toxicity features
CNS: agitation, tremor, anxiety, confusion, somnolence, syncope, hallucinations, changes in perception, acute psychosis, nystagmus, convulsions and coma. Cardiac: tachycardia, hypertension, chest pain, palpitations, ECG changes. Renal: acute kidney injury. Muscular: hypertonia, myoclonus, muscle jerking and myalgia. Other: cold extremities, dry mouth, dyspnoea, mydriasis, vomiting and hypokalaemia
272
Cocaine toxicity
Blocks the uptake of dopamine, noradrenaline and serotonin
273
Adverse cariovascular effects of cocaine
coronary artery spasm → myocardial ischaemia/infarction both tachycardia and bradycardia may occur hypertension QRS widening and QT prolongation aortic dissection
274
Cocaine neurological features
seizures mydriasis hypertonia hyperreflexia
275
Cocaine psychiatric effects
agitation psychosis hallucinations
276
Other effects of cocaine
ischaemic colitis is recognised in patients following cocaine ingestion. This should be considered if patients complain of abdominal pain or rectal bleeding hyperthermia metabolic acidosis rhabdomyolysis
277
Management of cocaine toxicity
- benzodiazepines -if with chest pain add GTN hypertension: benzodiazepines + sodium nitroprusside
278
MDMA poisioning
Ecstacy
279
Clinical features of Ecstasy poisoning
neurological: agitation, anxiety, confusion, ataxia cardiovascular: tachycardia, hypertension hyponatraemia this may result from either syndrome of inappropriate ADH secretion or excessive water consumption whilst taking MDMA hyperthermia rhabdomyolysis
280
Management of ecstasy poisoning
supportive dantrolene may be used for hyperthermia if simple measures fail
281
Exacerbation of chronic bronchitis
Amoxicillin Tetracycline Clarithromycin
282
Uncomplicated community-acquired pneumonia
Amoxicillin (Doxycycline or clarithromycin in penicillin allergic, add flucloxacillin if staphylococci suspected e.g. In influenza)
283
Pneumonia possibly caused by atypical pathogens
Clarithromycin
284
Hospital acquired pneumonia
Within 5 days of admission: co-amoxiclav or cefuroxime More than 5 days after admission: piperacillin with tazobactam OR a broad-spectrum cephalosporin (e.g. ceftazidime) OR a quinolone (e.g. ciprofloxacin)
285
Lower urinary tract infection
Nitrofurantoin or trimethoprim Alternative amoxicillin or cephalosporin
286
Acute pyelonephritis
Broad-spectrum cephalosporin or quinolone
287
# antibiotics Acute prostatitis
Quinolone or trimethoprim
288
Impetigo
Topical hydrogen peroxide, oral flucloxacillin or erythromycin if widespread
289
Cellulitis
Flucloxacillin (clarithromycin, erythromycin or doxycycline if penicillin-allergic)
290
Cellulitis near eyes or nose
Co-amoxiclav (clarithromycin, + metronidazole if penicillin-allergic)
291
Erysipelas
Flucloxacillin* (clarithromycin, erythromycin or doxycycline if penicillin-allergic)
292
Animal or human bite
Co-amoxiclav (doxycycline + metronidazole if penicillin-allergic)
293
Mastitis during breast-feeding
Flucloxacillin
294
Throat infection
Phenoxymethylpenicillin (erythromycin alone if penicillin-allergic)
295
Sinusitis
Phenoxymethylpenicillin
296
Otitis media
Amoxicillin (erythromycin if penicillin-allergic)
297
Otitis external
Flucloxacillin (erythromycin if penicillin-allergic)
298
Periapical or periodontal abscess
Amoxicillin
299
# antibiotics Gingivitis: acute necrotising ulcerative
Metronidazole
300
Gonorrhoea
Intramuscular ceftriaxone
301
Chlamydia antibiotics
Doxycycline or azithromycin
302
Pelvic inflammatory disease
Oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline and oral metronidazole
303
Syphilis treatment
Benzathine benzylpenicillin Doxycycline Erythromycin
304
Bacterial vaginosis
Oral or topical metronidazole Topical clindamycin
305
Clostridioides difficile
First episode: oral vancomycin Second or subsequent: oral fidaxomicin
306
Campylobacter enteritis
Clarithromycin
307
Salmonella (non-typhoid) AB
Ciprofloxacin
308
Shigellosis
Ciprofloxacin
309
Acute upper GI bleed
- common, usually caused by oesophageal varicose or peptic ulcer disease
310
Clinical features of GI bleeds
- haematemesis the most common presenting feature often bright red but may sometimes be described as 'coffee gound' melena the passage of altered blood per rectum typically black and 'tarry' a raised urea may be seen due to the 'protein meal' of the blood features associated with a particular diagnosis e,g, oesophageal varices: stigmata of chronic liver disease peptic ulcer disease: abdominal pain
311
Oesophageal varicose
Usually a large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.
312
Oesophagitis
Small volume of fresh blood, often streaking vomit. Malena rare. Often ceases spontaneously. Usually history of antecedent GORD type symptoms.
313
Oesophageal Cancer
Usually small volume of blood, except as a preterminal event with erosion of major vessels. Often associated symptoms of dysphagia and constitutional symptoms such as weight loss. May be recurrent until malignancy managed.
314
Mallory Weiss tear
Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting. Malena rare. Usually ceases spontaneously.
315
Gastric ulcer
Small low volume bleeds are more common so would tend to present as iron deficiency anaemia. Erosion into a significant vessel may produce considerable haemorrhage and haematemesis.
316
Gastric cancer
Frank haematamesis or altered blood mixed into vomit Usual prodromal features of dyspepsia and constitutional bleeding Amount of bleeding variable but erosion of major vessel may produce considerable haemorrhage.
317
Dieulafoy lesion
Often no prodromal features prior to haematemesis and melena, but this arteriovenous malformation may produce quite a considerable haemorrhage and may be difficult to detect endoscopically
318
Diffuse erosive gastritis
Usually haematemesis and epigastric discomfort. Usually there is an underlying cause such as recent NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise
319
Duodenal ulcer
These are usually posteriorly sited and may erode the gastroduodenal artery. However, ulcers at any site in the duodenum may present with haematemesis, melena and epigastric discomfort. The pain of a duodenal ulcer is slightly different to that of gastric ulcers and often occurs several hours after eating. Periampullary tumours may bleed but these are rare.
320
Aorto-enteric fistula
In patients with previous abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but important cause of major haemorrhage associated with high mortality.
321
Managment of GI bleeds
NICE guidelines 2012 the Glasgow-Blatchford score at first assessment helps clinicians decide whether patient patients can be managed as outpatients or not the Rockall score is used after endoscopy provides a percentage risk of rebleeding and mortality includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage
322
Blactchford score 0
Patients may be considered for an early discharge
323
Resus for patients with bleeds
ABC, wide-bore intravenous access * 2 platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal prothrombin complex concentrate to patients who are taking warfarin and actively bleeding
324
Endoscopy in upper GI bleeds
should be offered immediately after resuscitation in patients with a severe bleed all patients should have endoscopy within 24 hours
325
Managment of non-variceal bleeds
NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected non-variceal upper gastrointestinal bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy if further bleeding then options include repeat endoscopy, interventional radiology and surgery
326
Managment of variceal bleeds
terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy) band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
327
Acute treatment of variceal haemorrhage
-ABC response then endoscopy - may need blood transfusion correct clotting: FFP, vitamin K, platelet transfusions may be required Vasoactive treatment: telipressin - Octreotide can be used although evidence shows telepressin is better Prophylactic IV antibiotics
328
Transjugular Intrahepatic porotsystemic shunt
Used if original methods of managment fail connects the hepatic vein to the portal vein exacerbation of hepatic encephalopathy is a common complication
329
Variceal haemorrhage prophylaxis
- propanalol - Endoscopic variceal band ligation (EVL) -TIPSS used if above doesn’t work
330
3rd nerve compression secondary to tentorial herniation
- unilateral dilated pupil - sluggish or fixed to light response
331
Poor CNS perfusion or Bilateral 3rd Nerve palsy
Pupils bilaterally dilated Light response sluggish or fixed
332
Optic nerve injury
Unilateral dilated or equally dilated Cross reactive (Marcus Gunn light response)
333
Opiates Pontine lesion Metabolic encephalopathy
Bilaterally constricted pupil Light response may be difficult to assess
334
Sympathetic pathway disruption
Fig
335
Mechanism of alcohol withdrawal
chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)
336
Features of alcohol withdrawal
-6-12 hours: tremor, sweating, tachycardia, anxiety -peak incidence of seizures at 36 hours -peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia
337
Basics of testicular torsion
-twist of the spermatic cord resulting in testicular ischaemia and necrosis. -most common in males aged between 10 and 30 (peak incidence 13-15 years)
338
Features of testicular torsion
-pain is usually severe and of sudden onset -the pain may be referred to the lower abdomen nausea and vomiting may be present -on examination, there is usually a swollen, tender testis retracted upwards. -The skin may be reddened cremasteric reflex is lost elevation of the testis does not ease the pain (Prehn's sign)
339
Managment of testicular torsion
treatment is with urgent surgical exploration if a torted testis is identified then both testis should be fixed as the condition of bell clapper testis is often bilateral.
340
Non-haemolytic febrile reaction
Thought to be caused by antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cell during storage
341
Features of Non-haemolytic febrile reactions
Fever, chills Red cell transfusion (1-2%) Platelet transfusion (10-30%)
342
Managment of non-haemolytic febrile reactions
Slow or stop the transfusion Paracetamol Monitor
343
blood minor allergic reactions
Thought to be caused by foreign plasma proteins
344
Features of blood minor allergic reactions
Thought to be caused by foreign plasma proteins Pruritus, urticaria
345
Managment of minor allergic reaction blood
Temporarily stop the transfusion Antihistamine Monitor
346
Blood producrs anaphylaxis
Can be caused by patients with IgA deficiency who have anti-IgA antibodies
347
features of blood product anaphylaxis
Hypotension, dyspnoea, wheezing, angioedema.
348
Managment of blood anaphylaxis
Stop the transfusion IM adrenaline ABC support oxygen fluids
349
Acute haemolytic reaction
ABO-incompatible blood e.g. secondary to human error
350
acute haemolytic reaction features
Fever, abdominal pain, hypotension
351
Managment of acute haemolytic reaction
Stop transfusion Confirm diagnosis check the identity of patient/name on blood product send blood for direct Coombs test, repeat typing and cross-matching Supportive care fluid resuscitation
352
Transfusion-associated circulatory overload (TACO)
xcessive rate of transfusion, pre-existing heart failure
353
Transfusion-associated circulatory overload (TACO) features
Pulmonary oedema, hypertension
354
Transfusion-associated circulatory overload (TACO) managment
Slow or stop transfusion Consider intravenous loop diuretic (e.g. furosemide) and oxygen
355
Transfusion-related acute lung injury (TRALI)
Non-cardiogenic pulmonary oedema thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood
356
Transfusion-related acute lung injury (TRALI) features
Hypoxia, pulmonary infiltrates on chest x-ray, fever, hypotension
357
Transfusion-related acute lung injury (TRALI) managment
Stop the transfusion Oxygen and supportive care
358
Survival rate of CPR in hospital
13-17%, albeit many survivors experience long-term disability.
359
survival rate outside of hospital
10% of individuals who experience cardiac arrest outside of a hospital setting survive, while the reported overall success rate of CPR ranges from 5% to 20%.
360
survival rate of CPR out of hosptial
* 10% of individuals who experience cardiac * overall success rate of CPR ranges from 5% to 20%.
360
Anterior cerebral artery
Contralateral hemiparesis and sensory loss, lower extremity > upper
361
Middle cerebral artery
Contralateral hemiparesis and sensory loss, upper extremity > lower Contralateral homonymous hemianopia Aphasia
362
Posterior cerebral artery
Contralateral homonymous hemianopia with macular sparing Visual agnosia
363
Weber's syndrome (branches of the posterior cerebral artery that supply the midbrain)
Ipsilateral CN III palsy Contralateral weakness of upper and lower extremity
364
Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)
Ipsilateral: facial pain and temperature loss Contralateral: limb/torso pain and temperature loss Ataxia, nystagmus
365
Anterior inferior cerebellar artery (lateral pontine syndrome)
Symptoms are similar to Wallenberg's ), but: Ipsilateral: facial paralysis and deafness
366
Retinal/ophthalmic artery
Amaurosis fugax
367
Basilar artery
'Locked-in' syndrome
368
Lacunar strokes
present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia strong association with hypertension common sites include the basal ganglia, thalamus and internal capsule
369
ROSIER score
Used to identify strokes in emergency settings. Key symptoms (1 point each): Asymmetrical facial/arm/leg weakness Speech disturbance Visual field defect Exclude: Loss of consciousness or seizure activity (-1 point each) Scoring: ≥1: Stroke likely → Urgent action needed <1: Stroke less likely
370
first line investigation for suspected stroke
Non-contrast CT head scan
371
Staphylococcal toxic shock syndrome
Severe systemic reaction to staphylococcal exotoxins, the TSST-1 superantigen toxin. Prominence in the early 1980s following a series of cases related to infected tampons.
372
Toxic shock syndrome symptoms
fever: temperature > 38.9ºC hypotension: systolic blood pressure < 90 mmHg diffuse erythematous rash desquamation of rash, especially of the palms and soles involvement of three or more organ systems: e.g. gastrointestinal (diarrhoea and vomiting), mucous membrane erythema, renal failure, hepatitis, thrombocytopenia, CNS involvement (e.g. confusion)
373
TSS management
removal of infection focus (e.g. retained tampon) IV fluids IV antibiotics
374
What is this?
TSS
375
Osteoporotic vertebral fracture
gradually decrease in bone mineral density, so increase likelihood of fragility Fractures are more likely due to fragility.
376
Osteoporosis epiemiology
more common in females than in males. 25% of women will have developed osteoporosis by the age of 80 . The prevalence of vertebral osteoporotic fractures is difficult to determine
377
Risk factor for Osteoporotic fracture
advancing age Previous history of a fragility fracture Frequent or prolonged use of glucocorticoids History of falls Family history of hip fracture ow BMI (< 18.5) Tobacco smoking High alcohol intake: > 14 units/week for women, > 21 units/week for men
378
signs of Osteoporosis
Loss of height: vertebral osteoporotic fractures of lead to compression of the spinal vertebrae hence a reduction in overall length of the spine and thus the patient becomes shorter Kyphosis (curvature of the spine) Localised tenderness on palpation of spinous processes at the fracture site