Clinical Scenarios Flashcards
Chest pain (MI)
Immediate management
Administer sublingual GTN (monitor BP for hypotension)
IV morphine with antiemetics if pain persists
300mg Aspirin and Clopidogrel 300mg
Anticoagulation - loading dose of enoxaparin or fondaparinux if NSTEMI
STEMO - Primary PCI with 120 minutes or thrombolysis if PCI unavailable
Chest pain - tension pneumothorax management?
Tension pneumothorax, if the person’s condition is life threatening:
Consider inserting a large-bore cannula through the second intercostal space in the mid-clavicular line, on the side of the pneumothorax.
Chest pain - acute pulmonary oedema management?
Give an intravenous diuretic (for example furosemide 40 mg to 80 mg, given slowly).
Give an intravenous opioid (for example diamorphine 2.5 mg to 5.0 mg, given slowly over 5 minutes).
Give an intravenous anti-emetic (for example metoclopramide 10 mg). This can be mixed with diamorphine.
Give a nitrate, either sublingually or buccally (for example GTN spray, two puffs).
How quickly should someone be seen with chest pain?
Same day assessment if pain in the last 12 hours
within 2 weeks if the person is pain free with chest pain more that 72 hours ago
Long term management of ACS?
Address complications such as arrhythmias, heart failure, or shock.
Dual antiplatelet therapy (e.g., aspirin + ticagrelor).
Statin (e.g., atorvastatin 80 mg), beta-blocker, and ACE inhibitor.
Lifestyle advice: smoking cessation, exercise, dietary modification.
Sepsis Initial approach?
ABCDE assessment
Bloods - FBC, U&Es, lactate, CRP, cultures
Sepsis initial management?
Follow the Sepsis Six:
Administer oxygen if required.
Take blood cultures.
Give IV antibiotics (broad-spectrum, e.g., piperacillin-tazobactam).
Administer IV fluids.
Measure lactate.
Monitor urine output (insert catheter if needed).
Escalate care early if signs of septic shock persist (e.g., ICU).
What is sepsis?
Sepsis, a life-threatening medical emergency, results from a dysregulated host response to infection, leading to systemic inflammation and organ dysfunction.
The latest consensus definitions, known as Sepsis-3, identify sepsis as an infection with a concurrent increase in the Sequential Organ Failure Assessment (SOFA) score by ≥2 points, while septic shock is defined by persisting hypotension despite fluid resuscitation, necessitating vasopressors to maintain a mean arterial pressure of ≥65 mmHg, and a serum lactate level >2 mmol/L.
The new guidelines recognise the following terms:
sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection
septic shock: a more severe form sepsis, technically defined as ‘in which circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone’*
AKI initial assessment
ABCDE assessment
Assess for ureic complications (pericarditis, pulmonary oedema)
assess volume status in C
Monitor potassium levels - ECG to look for signs of hyperkalaemia
Initial management of AKI?
Hyperkalaemia - stabilize the myocardium with IV calcium gluconate
Shift potassium intracellularly with IV insulin and dextrose
Dialysis if required
Volume status
If hypovolaemic - IV fluids
If overloaded - consider diuretics
Stop nephrotoxic drugs
Investigations for AKI?
Urinalysis - check for blood, protein or casts
ECG monitoring
U&E’s bicarbonate and phosphate
Assess for causes - FBC (anaemia/infecion), CK (rhabdo) or immunological markers (ANA, ANCA)
anti GBM
complement levels
Immunoglobulin levels
A
Renal USS
causes for AKI?
Pre-renal - reduction in renal perfusion - Prolonged prerenal states, if not rectified, can progress to ATN, causing intrinsic renal damage.
Intrinsic
- Acute tubular necrosis
- Glomerulopathies
Interstitial disease
Vascular causes
Post renal
- obstruction
- back flow of urine
What are notifiable diseases?
Hep A/B/C
Acute meningitis
Acute Poliomyelitis
Anthrax
Botulism
Brucellosis
Cholera
Diphtheria
Enteric fever (typhoid/paratyphoid)
Haemolytic uraemia syndrome
Infectious bloody diarrhoea
Ivasive Group A strep
Legionnaires disease
Leprosy
Malaria
measles
Monkey pox
Plague
Mumps
Rabies
Rubella
Severe acute respiratory distress syndrome
Scarlet fever
Smallpox
Tetanus
Tuberculosis
Thymus
Viral hemorrhagic fever
whopping cough
yellow fever
Do not wait for laboratory confirmation of the disease. By law, you must report any suspicion of a notifiable disease
clinical signs of DVT?
Tenderness and firmness of the calf on palpation
Calf pain on dorsiflexion – known as Homans sign
Discolouration of the peripheral foot
Swelling of the affected leg which I would measure against the contralateral leg
Differentials for asthma attack in a young person
Pneumonia/infections
Pneumothorax
Anaphylaxis/allergic reaction
Heart failure due to cardiomyopathy and pulmonary arterial hypertension - this should always be considered in a young adult with new onset breathlessness.
what do you need to consider when assessing someone admitted with acute asthma attack?
When assessing a patient with an exacerbation of asthma it is essential to identify the severity of the asthma attack, as per the British Thoracic Society guidelines
Exacerbations can be divided into moderate, severe and life-threatening attacks. This is determined by the peak expiratory flow (PEF) in addition to other metrics. For a moderate exacerbation PEF >50–75% best or predicted; in a severe exacerbation PEF 33–50% best or predicted; and in a life-threatening attack PEF <33% best or predicted. Other signs that this is a life-threatening asthma exacerbation include:
SpO2 <92%
PaO2 <8 kPa
Normal PaCO2 (4.6-6.0)
Altered level of consciousness
Exhaustion
Arrhythmia
Hypotension
Cyanosis
Silent chest
Poor respiratory effort
There is a new category included in the 2019 British Thoracic Society Asthma Guidelines called “near-fatal” asthma exacerbation, which refers to an attack where there is a raised PaCO₂ and/or requiring mechanical ventilation with raised inflation pressures.
things to remember in A-E in asthma attack
B - assess for signs of respiratory distress such as severe breathlessness, cyanosis, silent chest, and a poor respiratory effort, as these are all signs of a life-threatening asthma exacerbation.
ABG and Peak flow would be crucial
Key to assess how the patient looks from the end of the bed - are they tiring - this is significant cause for cancer
Management of life threatening asthma
urgent treatment in an acute hospital setting
Nebulised beta 2 agonist via an oxygen driven nebuliser
If no response I would ask the nurses to give a second - back to back.
Steroids should be given - in life threatening could be given as IV hydrocortisone if patient can’t take oral
Can add ipratropium
IV magnesium - but would discuss with senior team member first
when to refer acute asthma to ITU?
As per the British Thoracic Guidelines, I would refer any patient that is:
requiring ventilatory support
with acute severe or life-threatening asthma, who is failing to respond to therapy, as evidenced by:
deteriorating PEF
persisting or worsening hypoxia
hypercapnia
ABG analysis showing decreasing pH or increasing H+
exhaustion, feeble respiration
drowsiness, confusion, altered conscious state
respiratory arrest.
updating a relative of a patient who has been taken to ITU?
Before speaking with the patient’s relative I would discuss the case with my consultant or senior registrar to be clear on the information I was going to communicate with them and so that I did not set unrealistic expectations or speak without fully understanding the situation.
Before speaking I would try and find a quiet space on the ward with chairs, to minimise interruptions, and hand over my bleep to one of my colleagues. I would ask the patient’s sister if there is anyone else they would like to be with them.
I would start our conversation by asking the sister what they already know and what they understand has happened. I would be clear about the order of events. When delivering bad news, I would ensure that I gave warning shots before, particularly when talking about cardiac arrest. I would make sure that I give appropriate pauses in my consultation for the relative to ask questions or take on board the information I am delivering. I would minimise my use of medical jargon and keep things simple.
When ending the consultation, I would check with the sister again if there is anyone else I need to speak to. I would offer her the chance to come to ITU and see her brother, once I had spoken to the ITU team. I would make sure that she is aware of other people on the ward she can speak with or how to get hold of me once we have finished, in case she has further questions.
REMEMBER WARNING SHOTS
Falls History
I would first start by asking about the falls. This would initially be with open questions – for example, how would the patient describe the fall?
- any dizziness or light headedness
- what were they dong leading up to the fall
- any LOC
- any injuries
- any associated symptoms - headache, visual disturbance, peripheral neuropathy
- were they able to get up off the floor or require assistance
- are all of the falls the same
think structure - before, during, after
PMH
Meds - any new medications, diabetic control
SH
Where does she live
what is mobility like
Systems review
Cognitive screening
Investigations for falls
L/S BP
ECG
Blood glucose
Bloods - FBC, Renal function, CRP, bone profile and vitamin D (rule out hypercalcaemia and can give bone protection to those who are falling)
24 hour ECG
Serial BP monitoring
Echo - if any murmurs on examination
if vestibular cause - could consider the dix0hallpike
would you order CT head for falls?
This would be based on my history, examination and investigation conducted in clinic. If there is a history of head injury associated with loss of consciousness or change in cognitive function, I would consider a CT head. If the patient is on any anticoagulant medication this would also change my thinking. I would discuss this request with my senior colleagues before ordering it.
Mrs Redbridge’s daughter tells you that she has recently been put on rivaroxaban for atrial fibrillation. After her first fall she hit her head and she has been increasingly confused. Would you order a CT head?
Yes I would order an urgent CT head that day to be performed whilst Mrs Redbridge is in clinic. I would be concerned about her having a subdural haematoma or intracranial bleed which could have occurred when she hit her head when falling with an increased risk due to her use of a direct-acting oral anticoagulant. She would meet the NICE criteria for arranging a CT head given her age profile and change in cognitive function.
Explaining SDH to patient?
I would start by making sure that we are in a quiet room where we will not be disturbed. I would ask the patient and daughter if there is anyone else that needs to be present.
WARNING SHOT!!!!!!!
I would start by explaining that the CT head scan has shown a cause for the worsening confusion. (This is the warning shot). I would then explain that the scan has shown a bleed around the outside of her brain.
Explain that the blood is likely exerting some pressure on the brain which is why Mrs Redbridge is more confused. The bleeding is likely secondary to her use of rivaroxaban which increases her risk of haematoma formation after head injury.
I would explain that the scans have been reviewed by my surgical colleagues who do not think that surgery is required.
Explain that Mrs Redbridge will be admitted for a short period to monitor and assess the impact of the bleed before being discharged home.
I would then make sure that the patient and family had time to ask questions.
explain to pt why not having surgery for SDH?
Should Rivaroxaban be stopped?
will my mother be safe to come home?
The surgeons have reviewed the scans. Decisions on surgery are made based on the presentation of the patient (is the bleed causing a threat to life), the success of surgery balanced against the risks. In this case, the risks of surgery would be high. The subdural haematoma will be resorbed slowly. We are monitoring to make sure that Mrs Redbridge remains stable.
Yes, we will stop the rivaroxaban today. This will reduce the likelihood of the bleed getting any bigger. A decision on restarting the rivaroxaban will be made with the senior clinician based on the risks and benefits of continuing to take it.
Your mother will be assessed by our inpatient therapy team during the admission to assess her current level of mobility and self-care. Based on this we make recommendations about her safety to go home on her own. She may need a reablement package of care for example depending on the outcome of the assessment.
TIA History Taking ?
I would initially start with open questions followed by more closed questioning to help me narrow my differential diagnosis. I would make sure that I use appropriate language and try to avoid medical jargon in my questions.
- when did it happen (time of day) and how long did it last
- exactly what symptoms occurred - weakness - distribution, difficulty with speech, slurring of words, change in sensation, visual impairment, impaired mobility, balance issues
- how long did they symptoms last
- have the symptoms completely resolved
- any warning symptoms
- what were they doing when it came one and events leading up to it
- any head trauma
- any change in consciousness
- any associated pain
- similar precious episodes
PMH
diabetes and HTN - are they well controlled
SH
smoking
alcohol
medications
FH of stroke
Important to ask if patient drives
finally I would finish with a systems review to identify any symptoms that the patient may have forgotten to say
Ask about ICE
Investigations for TIA
determined by the history and examination
Full set of observations
L/S BP
ECG
Bloods - FBC, Renal profile, HbA1c, lipid profile
further include 24 hour ECG, echo, carotid USS and MRI head
I would want to discuss with my consultant
Differentials for TIA?
Toxic/metabolic disturbance - hypoglycaemia, drug and alcohol toxicity
Neurological - seizure, migraine with aura, MS, peripheral neuropathies such as Bell’s palsy
Systemic or local infection - central nervous system abscess, encephalitis, sepsis
Space occupying lesion - tumour, subdural haematoma
Conditions which can cause dizziness or disturbed balance such as:
Syncope.
Labyrinthine disorders — vertigo, Meniere’s disease, labyrinthitis.
Encephalopathies such as:
Hypertensive encephalopathy.
Wernicke’s encephalopathy.
Others - acute confusional state, dementia, vasculitis, somatoform or conversion disorder
You confirm a TIA based on your history and investigations. What advice would you give to the patient and what treatments would you start in clinic?
I would begin by explaining to the patient what a TIA is. I would explain that a transient ischaemic attack (TIA) is often a herald of a stroke. The mainstay of treatment is about prevention of a stroke following the TIA. The patient should be advised on lifestyle measures including encouraging physical activity; advice around stopping smoking and referral to smoking cessation services if indicated; advice on a healthy diet – low salt, reduced intake of saturated fats. Advice should be given about drinking alcohol with consumption limited to less than 14 units a week.
With regards to treatment, antiplatelet therapy should be started if the patient is not already on it. Currently, dual antiplateley therapy is recommended of clopidogrel and aspirin for 21 days, followed by monotherapy with clopidogrel. Other options are available if this is not tolerated. Unless contraindicated, treatment with a high intensity statin should be initiated, such as atorvastatin 80mg OD. Cholesterol should be checked three months after initiating this to check the response to medication.
The patient is likely already on anti-hypertensive medication but if not this should be considered in the clinic with a target systolic blood pressure of below 130 mmHg (unless there is severe bilateral carotid stenosis). Making sure his diabetes is well managed will also be an important part of his stroke prevention
I would make sure that I discuss all medication decisions with my clinical supervisor in the clinic.
Explaining to patient they ate being started on DOAC?
Direct oral anticoagulants (DOACs) are drugs which prevent harmful blood clots from forming in your blood vessels. They do this by slowing down the clotting process. They have a similar effect on thinning the blood as warfarin.
The medication is taken each day. It is important to take the medication at the same time each day to ensure that they work properly. If you miss a dose, you should take the medication as soon as you remember if on the same day, however, you should not take two tablets on the same day.
There are several side effects associated with a DOAC that it is important for you to be aware of. If you experience these, you should seek medical attention: prolonged nosebleed; bleeding from cuts; blood in your stool/vomit/sputum/urine; spontaneous bruising; persistent headache. You should seek emergency medical attention if you suffer any major trauma or head injury.
DOACs do not need monitoring (in the same way as warfarin). However, kidney function should be checked prior to starting the medication and may need to be reviewed if there is any change in this.
DOACs do not interact with alcohol. However, I would advise minimal alcohol intake when taking a DOAC because of alcohol on your balance/walking and the increased likelihood of head injury when intoxicated.
I’m happy to provide you with written information on the drug so that you can read it at your own pace prior to starting the medication so that you can make an informed choice. If you choose not to take the medication the risk of further cerebrovascular events because of the atrial fibrillation will be higher - taking blood thinners reduces your risk by as much of two-thirds (https://pubmed.ncbi.nlm.nih.gov/22514252/) Use of the DOAC tablets in patients with AF reduces the risk of a severe stroke by about 50% compared to those taking warfarin, which is the older drug. (https://www.ahajournals.org/doi/10.1161/STROKEAHA.119.025554)
treatment of AF following TIA ?
Anticoagulation should be initiated in patients who present with TIA who are found to have persistent or paroxysmal atrial fibrillation. Treatment can start as soon as imaging has confirmed no presence of haemorrhage or factors that may be contraindicated – for example the presence of microhaemorrhages in cerebral amyloid angiopathy.
The risk of bleeding when considering starting anticoagulation can be assessed using the ORBIT bleeding risk tool
The choice of anticoagulant is likely to be determined by local policy and I would discuss this with my clinical supervisor in the clinic.
TIA and Driving
People who have had a TIA must not drive for one month, but they do not need to inform the DVLA. If the patient has a further TIA, then they should stop driving for 3 months and inform the DVLA at this point.
SBAR handover for TIA in TIA clinic?
S: I have just assessed Mr Adene, a 69-year-old gentleman, who was referred to clinic following a transient episode of right hemiparesis and word finding difficulty.
B: He has a background of hypertension, type two diabetes, and COPD.
A: Based on my assessment I believe that the presentation is consistent with a transient Ischaemic Attack. I have arranged several investigations to help identify the source of the TIA and based on an ECG in clinic we have also confirmed a diagnosis of atrial fibrillation. I have spoken with Mr Adene about prevention of future stroke including lifestyle measures and have started him on high dose statin. Because of the atrial fibrillation I believe that Mr Adene would benefit from being on long term anticoagulation and have discussed this with the patient. I have spoken with him about driving and when he can return to this.
R: Mr Adene should be followed up in this clinic to check his response to the medications initiated today and to review the outcome of further investigations that I have arranged including his prolonged ECG monitoring and his MRI head so that a DOAC can be started safely. I have made sure to safety net and informed Mr Adene to present back to hospital should he have any recurrence of his presenting symptoms.
Not being able to attend teaching due to short staffing
he balance of training vs service provision can often fall unfavourably
There is a moral and practical obligation to ensure juniors such as yourself are trained appropriately to form the next generation of senior doctors. Missing regular teaching opportunities could result in a lack of personal and professional development and ultimately prevent you from performing at the expected level of a registrar at the end of your training.
This of course needs to be balanced against the short-term patient safety issues that could be raised by you leaving what sounds like a very busy ward. If this situation has arisen due to a genuine medical emergency then clearly it would be inappropriate to leave the ward for teaching but this is unlikely to be the case on multiple occasions and instead likely represents a cultural or staffing issue in the department.
Not being able to go to teaching - who could you escalate it to?
You need to immediately raise your concerns with the consultant in question and if they are not willing to help, it may need to go further and involve other external figures such as your clinical supervisor (if this is a separate person) or your educational supervisor. If this is unsuccessful or the situation remains unresolved despite this, further escalation to your training programme director or head of department may help to resolve the situation.
It may be that the consultant themself has been under considerable pressure and has neglected to think of how the situation has affected you, in which case simply explaining why it is inappropriate could help.
You can also submit an ‘exception report’ to make a paper trail of missed training opportunities (in addition to staying late at work) which would highlight the issue at an organisational level.
Do consultants have a contractual obligation to help facilitate teaching for junior trainees?
It is a professional and contractual requirement for consultants working in areas with trainees to help facilitate their education and training. Many consultants will understand this and be keen to help contribute to your learning but in other cases may need stronger reminders of the importance of teaching.
investigations for cough/wheeze/SOB
observations
sputum sample
ECG
Bloods (raised Hb in response to chronic hypoxia)
renal function CRP
CXR (in COPD may have hyper inflated lungs and flattened diaphragm)
PEF
Spirometry
Echo
CT chest
Differentials for for cough/wheeze/SOB
Asthma
Bronchiectasis
Lung cancer
Tuberculosis
Congestive heart failure
Medication induced]
Gastro-oesophageal reflux disease
COPD in lay terms
COPD is a long-term lung condition that makes it hard to breathe. It happens because the airways (the tubes that carry air in and out of your lungs) become inflamed, damaged, and narrowed, and the air sacs in your lungs (which help transfer oxygen to your blood) don’t work as well as they should.
Brochiectasis in lay terms
Bronchiectasis is a chronic lung condition characterized by irreversible dilation and damage to the bronchi, the airways responsible for carrying air to and from the lungs. This structural abnormality leads to impaired clearance of mucus, recurrent infections, and inflammation.
explaining COPD to patient?
Hi Mrs Bruth. I wanted to talk to you about the results of the investigations that we have ordered. These have come back and shown the reason for your cough, wheeze and shortness of breath.
The scans have confirmed a diagnosis of Chronic Obstructive Pulmonary Disorder. Have you ever heard of this before? Some people will also refer to this as emphysema or chronic bronchitis (It is worth giving the patient time – they may want to respond or will indicate time for you to keep going. Pausing and giving the patient time to take in your words is an important part of communication).
Would you like me to explain a little bit about what this diagnosis means?
Chronic Obstructive Pulmonary disorder (or COPD for short) is a disease of the lungs which results in damage and inflammation to the airways that makes it harder for you to get air in and out which results in feeling short of breath. It is a progressive disorder and the inflammation of the airways is not reversible (such as in asthma).
COPD is common in the UK. The majority of cases are caused by long term smoking, although air pollution is also a common causative factor.
Symptoms can be managed with a combination of inhalers which we will start today and I will ask the respiratory CNS to talk to you in more detail about inhaler technique. The main thing that you can do which will help with slowing the progression of disease is to stop smoking. Exercise and losing weight will also help the condition.
COPD is a chronic condition, but you can experience exacerbations of your symptoms which may be prompted by viral infections for example. Exacerbations may require management with antibiotics and in extreme cases oxygen.
Does what I have told you make sense? Do you have any questions?
Depending on what you have said, you may be asked various follow up questions. These could range from treatment advice to asking about cancer to long term prognosis. Remember, you are not expected to know everything. All you are being judged on is your ability to communicate, so stay calm and answer in a polite way. Anything you don’t know you can say and demonstrate how you would go about finding the answer.
Finally:
I will provide you with written information on COPD. I will be referring you to the community respiratory team who will be responsible for your ongoing management of COPD and they along with your GP will be good points of contact moving forward.
Management of severe hyperkalaemia?
Send serum potassium (U&E) and ask for ECG (although this should not delay treatment)
Calcium gluconate (stabilise cardiac myocytes)
Salbutamol nebs
Insulin/dextrose infusion
Cardiac monitoring
Look for a cause… (renal failure, exogenous potassium, spironolactone)
Calcium resonium not required for immediate management
causes of AKI
Causes of AKI can be split into pre-renal, renal and post-renal
Pre-renal: volume depletion (most common), heart failure, liver failure, low BP
Renal: RTA, trauma, contrast induced nephropathy, glomerulonephritis
Post-renal: stones, BPH, malignancy, BOO, catheter problems
You commence treatment and repeat the potassium after 2 hours. The VBG result is 7.1 and there is now a metabolic acidosis. How do you proceed?
State your recognition of the refractory hyperkalaemia. Say you would reassess the patient A to E. Has treatment been given? Is the cannula working? Is there any exogenous potassium being given to the patient? Send repeat serum sample to confirm diagnosis. -could consider sending a slow spin.
Involve medical registrar – seeking senior support is essential as this patient is not improving but also is at risk of further deterioration
Move patient to HDU/resus setting
Involve ITU registrar
Indications for dialysis?
Refractory hyperkalaemia
Metabolic acidosis
CKD Stage 5
Fluid overload unresponsive to treatment
Symptoms of uraemia
how can you group differentials?
VITAMIN CDEF useful aide-memoire (V-vascular I-infective T-trauma A-autoimmune M-metabolic I-iatrogenic N-neoplastic C-congenital D-degenerative E-endocrine F-functional)
causes of PR bleeding?
Causes of PR bleeding can be broken down into local and systemic.
Local causes include haemorrhoids, anal fissures and fistulas.
More proximal causes can then be divided according to their underlying aetiology:
Vascular: mesenteric ischaemia, angiodysplasia
Infective: gastroenteritis
Neoplastic: anal cancer, colorectal cancer
Inflammatory: diverticulitis, Crohn’s disease, Ulcerative colitis
AF and PR bleeding - what are you worried about?
Given the patient’s age and her past medical history of atrial fibrillation, from the list of differentials I am immediately concerned about mesenteric ischaemia. Her age also puts her at risk of diverticulitis and colorectal cancer.
History for PR bleeding?
I would begin with a detailed history of the presenting complaint: onset, nature (colour, volume, etc) which may provide an indication as to the severity and aetiology.
I would also ask how the patient has been in herself recent (recent infection, systemic symptoms- weight loss, fever, lethargy) or any previous similar episodes. If concerned about gastroenteritis I may also enquire about infective contacts (i.e. other residents), any potential food sources or recent antibiotics courses (clostridium difficile).
PMH: I would ask specifically about past gastrointestinal conditions such as previous diagnoses of diverticulitis or IBD.
Dx: I would check if she takes antiplatelets or anticoagulants especially as these may be indicated from the PMH.
Other risk factors for the differentials would include a family history of clotting disorders or gastrointestinal conditions with familial components to the aetiology (colorectal cancer, IBD) and general social history (smoking history, diet/lifestyle- risk factors for malignancy).
An important consideration would also be a social history, to provide more information about this patient’s functional status. This is important because she is at risk of becoming critically unwell, and if so there may need to be conversations with the critical care team about escalation to ITU, and whether this would be appropriate.
Investigations for PR bleeding
Bedside - ECG, PR exam, stool cultures, ABG/VBG
Bloods - FBC, U&E’s, LFTs, clotting profile, group and save
Imaging - if any concerns about obstruction or toxic mega colon I could consider abdominal XR (risk in UC and C.diff)
Erect CXR if any concerns about perforation.
If haemodynamically unstable - urgent CT angiogram once the patient has been resuscitated. I would discuss this with my seniors
Her arterial blood gas results are now available: pH 7.28 PaO2 10.5kPa PaC02 4kPa Bicarbonate 15 Base excess -4 Lactate 4.5. How would you manage her?
The arterial blood gas shows a metabolic acidosis with a raised lactate. There is acid base disturbance with signs of hypoperfusion. This is immediately concerning. I would begin the patient on fluids if she is not already on fluids. Providing there are no contraindications I would initiate a fluid challenge starting with 500ml of a crystalloid fluid such as Normal Saline 0.9% ran STAT and would then reassess, continuing as necessary.
PR bleeding with raised lactate an metabolic acidosis - who do you want to inform?
Senior colleague and ask them to review
ensure the team looking after her are aware - ED consultant and nurse
Discuss with the surgical team
If not deteriorating - discuss with ITU
If rapidly deteriorating discuss - 2222/MET team
please hand over patient with PR bleeding, raised lactate and metabolic acidosis?
Situation: I am concerned about this 82 year old lady with a raised lactate and metabolic acidosis secondary to hypoperfusion as a result of a significant PR-bleed.
Background: She has a history of persistent pr-bleeding and is also known to have AF. Her drug history is not known.
Assessment: Fluid resuscitation has been started and a group and save ad crossmatch has been urgently sent to the lab. She is tachycardiac and hypotensive.
Recommendations: I am worried that this patient could quickly deteriorate. I have recommended that she is moved to the Resus department in A+E where she can be closely monitored. She needs an urgent senior review. I have asked the team to urgently request her drug history from the nursing home. If she is on anticoagulation for her AF she may need a reversal agent or discussion with haematology. In the event of a further deterioration she should be given O-negative blood from the transfusion fridge pending her formal cross-matched sample.
Given the presentation and her continued deterioration, she may benefit from being reviewed by the general surgical team.
Pleuritic chest pain assessment
remember -
If appears severely breathless - immediately start 15L NRB
Remember to assess for effort of breathing and respiratory distress
C - JVP and skin turgor
assess fluid status
monitor urine output - may require catheterisation
At the end - if I had any concerns I would want to escalate this to a senior
Her observations are: oxygen saturations 94% on room airA RR 32, HR 110, BP 90/60, T 38.0 What investigations would you do?
REMEMBER SEPSIS
COMMENCE SEPSIS 6
I am concerned that this patient may be septic. I would therefore ensure a sepsis six is completed. This includes checking a lactate, and taking blood cultures. I would also ensure urine output is monitored (with a catheter if necessary), and that fluids, IV antibiotics and oxygen are administered.
Bloods
ABG
ECG
CXR
Sputum sample
Urine dip - for atypical antigens
Here are the results of some investigations. Bloods Hb 130 g/dL, WBC 16 x 10^9/L, Neut 13 x 10^9/L, Plt 500 x 10^9/L, CRP 75, Urea 17 mmol/L, D-dimer 1.76 (0.1-0.45mg/L), CXR: Hazy opacification in the left lower zone, ECG Sinus tachycardia. Please interpret them.
How would you interpret the D-dimer result?
The bloods demonstrated a high white cell count which is predominantly a neutrophilia, supporting the diagnosis of a bacterial infection such as community acquired pneumonia. Both platelets and CRP are elevated, also indicating an inflammatory response. The elevated urea suggests her hypotension is causing poor kidney flow.
The D-dimer is elevated, which can suggest DVT or PE however can be elevated for several reasons and may be in keeping with pneumonia.
CXR is again supportive of pneumonia.
The results are supportive of community acquired pneumonia so I would continue to treat this, and continue fluid resuscitation. The elevated dimer is a complication which I would discuss with my registrar for consideration of a CTPA to rule out a PE.
What is your approach to using and interpreting D-dimers?
A D-dimer may not initially be helpful as it has a low specificity of 45%, i.e. can be positive for many reasons, e.g. obstetrics, peripheral vascular disease, cancer, inflammatory diseases and increasing age.
However, it can be used in conjunction with the modified Wells’ score. A patient can be scored and if they are low risk a (negative) D-dimer may be used to rule out a pulmonary embolism. Patients at higher risk of PE should not have a D-dimer and a CTPA should be performed as the first line investigation
In this case I would therefore consider performing a CTPA to rule out a pulmonary embolism.
What input would intensive care provide?
Intensive care would be able to provide a higher level of care with intensive nursing and closer monitoring and management from clinicians. In the acute phase ITU may be able to provide an arterial line to facilitate frequent arterial gas sampling for lactate monitoring, and venous lines for intensive fluid replacement and monitoring. If required they would be able to facilitate use of vasopressors or intubation and ventilation.
Assessment of severity in pneumonia?
each score one
confusion
BUN > 19/> 7
RR >. 30
BP < 90 or diastolic < 50
Age > 65
patient with CAP - deteriorating - What would you say to the patient if they were in front of you now?
- ensure privacy
– introduce myself and my role - ask if there was anyone else she wanted there
- explain in simple language that we are treating for a bad chest infection and that she needs to stay in hospital
- treating with Abx and fluids
- ask if she had any questions at any point
- ask if she wanted me call anyone and inform them
what is the new criteria for sepsis?
qSOFA
A bedside screening tool that consists of three simple tests:
Altered mental status
Systolic blood pressure less than or equal to 100 mm Hg
Respiratory rate greater than or equal to 22 breaths per minute
Patients with two or more of these findings should be examined for organ dysfunction.
things to remember in B and C of a-e assessment
b - it is vital to diagnose and treat immediately life-threatening conditions (e.g. acute severe asthma, pulmonary oedema, tension pneumothorax, and massive haemothorax).
c- if septic - start sepsis 6 at this stage
- IV abx, fluids, oxygen
- lactate, blood cultures, monitor urine output
at the end - consideration of escalation status if they are elderly
? do they already have an ACP
Define Sepsis and septic shock
Sepsis as a life-threatening organ dysfunction due to a dysregulated host response to infection.
Sepsis is a life-threatening condition that arises when the body’s response to an infection causes widespread inflammation, tissue damage, and organ dysfunction
Septic shock is a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality.
Septic shock is a severe form of sepsis characterized by persistent low blood pressure (hypotension) that does not improve with fluid resuscitation and requires vasopressor medications to maintain adequate blood pressure and perfusion.
what is sepsis 6
The sepsis six was a name given to a bundle of therapies designed to reduce the mortality of patients with sepsis. It was not included in the updated version of the Surviving Sepsis Campaign Bundle but was adapted. However, it is still routinely used in hospitals when responding to patients with possible sepsis. It includes:
Titrate oxygen to a saturation target of 94%
Take blood cultures
Administer empiric intravenous antibiotics
Measure serum lactate and send full blood count
Start intravenous fluid
Commence accurate urine output measurement
risk factors for sepsis ?
Key risk factors that would make you more susceptible to sepsis include: underlying malignancy, age older than 65 years, immunocompromise, haemodialysis, alcoholism, and diabetes mellitus.
The patient in this case is at risk due to her older age.
Prognosis for sepsis?
The prognosis in patients with sepsis and septic shock is guarded at best. The mortality rate from sepsis has been estimated in a number of studies to be between 28% and 50%.
The SOAP study in Europe observed an overall hospital mortality of 36%.
causes for reduced GCS?
Toxic causes such as opiate use, alcohol, anxiolytics, antidepressants
Metabolic causes such as hypoglycaemia or electrolyte disturbance
Trauma - i.e.head injury
A vascular event – such as an intracranial haemorrhage or large territory infarct
Infective causes such as meningitis or encephalitis. Given there is evidence of vomiting he is also at risk of aspiration pneumonia
Neurological causes - the patient could be post-ictal following a seizure.
Addisons crisis bloods
hyponatraemia
hyperkalaemia
hypoglycaemia
causes of hypoglycaemia ?
drugs and alcohol are the main causes
most common drugs - insulin and sulfonylureas
rarer drugs - salicylates, beta blocker, quinine and pentamidine
Organ failure, acute liver failure, adrenal failure, myxoedema, hypopituitarism, due to infection e.g. malaria
The high potassium and low sodium on the blood gas results would in particular raise suspicion of an acute adrenal crisis
If worried about adrenal insufficiency - should decide if IV steroids be given
rarely - insulinoma
In the A&E department you are unable to give IV glucose as access is incredibly difficult. You ask the nurse to give IM glucagon however there is no response in blood glucose. What is the cause of this patient’s hypoglycaemia?
Glucagon is a hormone that induces conversion of glycogen to glucose in the liver, thereby raising the blood glucose level.
The fact that glucagon has not worked would suggest that the process of glycogenolysis is not working. This would indicate that the cause of the hypoglycaemia is due to the inhibition of liver cells, most likely due to acute excessive alcohol consumption. This is the likely cause for the patient’s presentation.
What information should be given to patients with diabetes who drink alcohol?
don’t drink too much
risk of hypoglycaemia
alcohol inhibits the liver’s ability to release glucose into the blood. This impairment can last for several hours after drinking alcohol.
eat before drinking
eat carbs before going to sleep
What information should be given to patients with diabetes about hypoglycaemic episodes?
educating on nutrition
checking blood glucose
signs and symptoms of hypoglycaemia
recognition of early symptoms is important
must inform DVLA if they drive and take insulin
Patients should always be encouraged to check their blood glucose before driving and take regular breaks to test their blood sugar. If the blood sugar is less than 5.0 mmol/L then patients should not drive. If they have a hypo they should treat it and not drive for at least 45 minutes, until blood sugars have returned to above 5.0 mmol/L.
why are vasodilators used in pulmonary oedema ?
to reduce preload and afterload, improving cardiac output.
Avoid if patients are hypotensive
