Episode Twenty-Three: Chronic Disease

  • Written and Researched By: Caleb Dusdal
  • Peer Review By: Sarah Donnelly

Objective One:
In a patient with a diagnosed chronic disease who presents with acute  symptoms, diagnose: acute complications of the chronic disease acute exacerbations of the disease

Diabetic Ketoacidosis

Who gets it?
Usually type 1 diabetes, but 10-30% of cases are newly diagnosed type 2.
Causes
One of the important things to include when diagnosing DKA is the ‘secondary to ___’ modifier, because it doesn’t just happen, it needs a catalyst.
Some of these causes are commonly recalled as the Seven I’s

  • Infection: pneumonia, bacteraemia, UTI, etc
  • Ischemia: ACS, critical limb ischaemia, or ischaemic bowel
  • Intoxication: EtOH, MDMA, Cocaine, Methamphetamines, etc
  • Infraction/Intolerance: refers to patient not taking their insulin for whatever reason
  • Iatrogenic: steroids, surgeries
  • Initial presentation: first time presentation, which is usually in children with type 1, but could also be a new T2DM presentation
  • Impregnation: due to the increased metabolic demands of pregnancy and anti-insulin nature of placental hormones

How do they present?
Clinical features relate to their: hyperglycaemia, volume depletion and acidosis

  • Osmotic diuresis will gradually lead to volume loss as well as losses of:
    • Sodium
    • Chloride
    • Potassium
    • Phosphorous
    • Calcium
    • Magnesium
  • Often polyuria and polydipsia are the only symptoms until ketonaemia and acidosis develop
    • Due to osmotic diuresis from elevated sugars in the serum
  • Stimulated respiration
    • From acidosis triggered to diminish excess pCO2 to counter the metabolic acidosis
  • Nausea and/or vomiting 
    • Thought to be secondary to prostaglandin release, and may also be a maladaptive physiologic response to acid load.
  • Impaired mental status
    • Which has been found to correlated more with hyperosmolarity than with severity of acidosis
  • Tachycardia, orthostasis, hypotension, poor skin turgor and dry mucous membranes
    • From volume depletion

Diagnosis
1. Blood glucose level > 13.8 mmol/L
2. An anion gap >10 (+-2) mmol/L
3. Bicarbonate level < 18 mmol/L, and
4. pH < 7.3
5. Presence of ketonuria or ketonaemia

**While still largely limited to case studies, one pathology to keep in mind is Euglycemic DKA, associated with SGLT2i, Keep aware as this is likely to become more common as these medications become more and more prescribed. If it walks and talks like a DKA, but without a high glucose, look at their med list and workup for DKA**

https://www.cfp.ca/content/62/9/725

Treatment
The details of this are going to differ depending on the center you are working in, but the overall strategy will not.
The goals of DKA treatment in order, are:

  1. Volume Repletion (this is for severe volume depletion)
    1. Often you are initiating 0.9% saline infusion even before, or concurrent with, labs being drawn.
    2. If they are in shock, 1-2L/h to correct the shock
    3. Otherwise, 500mL/h for 4 hours, then 250mL/h for 4 hours, then, as required
    4. If the blood glucose falls to 14 mmol/L, you need to add glucose such as 0.45% saline with 5% dextrose, to keep it between 12-14mmol/L because the goal is not to correct the glucose, but the ketosis, so keep the serum glucose above 12 until your anion gap is closed
  2. Reversal of metabolic consequence of insulin insufficiency
    1. Before you initiate an insulin infusion, you need to assess the K+ level. This is because insulin is going to pull K+ with the glucose into the cells, and your K+ is going to drop, often into dangerous levels of hypokalaemia.
      1. If your K+ is > 5.2, then you can start the insulin infusion, usually 0.1U/kg/h
      2. If your K+ is between 3.3 and 5.2, then add 20-40mEq of K to each litre of your fluids, and initiate your insulin infusion
      3. If the K is under 3.3, don’t give insulin, but supplement your fluids with 20-40mEq of K, until it is above 3.3 mmol/L.
    2. Your insulin infusion is to continue until a few variables are met so you can transition to SC insulin, these are:
      1. Serum bicarb > 15mEq/L
      2. pH > 7.3
      3. And a normal anion gap
    3. Monitor labs q1-2hrs during this period
  3. Correction of electrolyte and acid-base imbalance
    1. In addition to the above:
      1. Only replace phosphate if less than 0.323 mmol/L otherwise don’t worry about it
      2. Only replace magnesium if less than 1 mmol/L, according to Tintinalli’s
      3. Only give bicarb if pH <= 6.9, otherwise, no role for it.
  4. Recognition and correction of precipitating cause
  5. Avoidance of complications

https://guidelines.diabetes.ca/cpg/chapter15

Hyperosmolar Hyperglycaemic State

Who gets it?
Usually a debilitated patient with poorly controlled, or undiagnosed type 2 diabetes, and commonly a precipitating illness.

Causes
Usually insulin resistance, or deficiency from chronic poorly controlled T2DM, plus
an inflammatory state with marked elevation in proinflammatory markers(eg CRP) and counterregulatory hormones (eg Cortisol)
plus
osmotic diuresis followed by impaired renal excretion of glucose, and often inadequate free fluid intake

  • You can also just think of the same triggers as we used for DKA

How do they present?
Usually elderly with co-morbidities referred by caretaker for vague abnormality in vitals, or mental status changes occurring over days or weeks. Sloooooow loooong onset.

  • Weakness, anorexia, fatigue, dyspnoea, chest or abdo pain
  • May also suggest the triggering condition such as a pneumonia or UTI

Physical exam items are non-specific as well:

  • Profound volume depletion (they are usually 10-12L negative)
    • Poor skin turgor, dry mucous membrane, sunken eyes, hypotension

Diagnosis

  • Often very severe hyperglycaemia compared to DKA, often > 33 mmol/L
  • Elevated serum osmolality > 315 mOsm/kg (per Diabetes Canada Guidelines > 320 mOsm/kg)
  • Unlike DKA, bicarb is > 15 mmol/L
  • Also unlike DKA, pH is > 7.3
  • And serum ketones are usually negative or only mildly positive

Treatment
The key to HHS is improvement of tissue perfusion, and often can see rapid correction with just fluid resuscitation, though most sources suggest you will still need insulin for significant hyperglycemia.

One variable that is different for HHS from DKA is that by definition, we won’t have an anion gap. As such our insulin infusion is modulated based on serum glucose (Tintinalli’s)

  • 0.1 U/kg/h infusion initially, assuming potassium is at least 3.3 per the DKA protocol
  • Goal is glucose reduction of 2.8 mmol/L/hr
    • If it falls more than 3.9 mmol/L/hr, then cut your insulin infusion into half or 0.05U/kg/hr

If it falls less than 2.8, then you can increase the infusion to .14-.2U/kg/hr

COPD Exacerbation

Defined as an acute worsening of respiratory symptoms in a human with COPD that results in a need for additional therapy.

Triggers for COPDe:

  • more than 75% of exacerbations have evidence of viral or bacterial infection
  • Hypoxia
  • Cold weather
  • Beta blockers
  • Narcotics, or sedative/hypnotics

What does it present with?

  • Hypoxaemia, <90% is the most life-threatening feature. Signs of hypoxaemia include:
    • Tachypnea
    • Tachycardia
    • HTN
    • Cyanosis
    • Change in mental status
  • Patient attempts to overcome severe dyspnoea/orthopnea by:
    • Sitting in an up and forward position
    • pursed -lip exhalation
    • Engaging accessory respiratory muscles
  • Pulsus paradoxus, which is a drop of more than 10mmHg sBP during inspiration 

Diagnosis
An COPD exacerbation is a clinic diagnosis made when a patient with COPD experiences a sustaining, 24-48hour increase in:

  1. Cough
  2. Sputum production
  3. and/or dyspneoa

For an excellent review of the most useful physical exam findings to help differentiate COPD from Acute heart failure (AHF), check out the COPD episode https://thegenerehlist.ca/2021/03/21/episode-eighteen-copd/ 

Treatment
The goal of course is to: correct oxygenation, alleviate bronchospasm and treat the underlying cause:

  1. correct tissue oxygenation, 
    1. Supplemental oxygen to raise the PaO2 above 60mmHg or SAT above 90%
    2. Non-invasive mechanical ventilation 
      1. Consider if:
        1. Worsening respiratory acidosis:
          1.  pH <7.36 with hypercapnia PaCO2 >50 on a gas and SAT <90%
            OR
        2. Severe dyspnoea with signs of respiratory fatigue or increasing work of breathing
    3. Corticosteroids, 5-7 days improved lung function and hypoxaemia and shorter time to recovery
  2. Alleviate reversible bronchospasm
    1. Short acting beta2-agonists(eg Salbutamol) are first line
      1. Given q30-60minutes if tolerated 0.5 mg, or 2.5mL of the 0.02% solution
      2. Can be given every 20 minutes, but this can result in more side effects like: tremor, anxiety, tachycardia, and palpitations.
    2. With or without short-acting anticholinergics(eg Ipratropium)
    3. Continuation of prescribed long-acting inhaled medications
  3. Treat the underlying cause
    The most common trigger is an infection, either viral or bacterial. And so, antibiotics are indicated if there is change in volume of sputum and an increased purulence character of the sputum.
    1. Check your local antibiogram or Spectrum app for recommended antibiotics, for me locally it is:
      1. For outpatient CAP
        1. Doxycycline, or Clarithromycin
      2. If you’re admitting for CAP
        1. Ceftriaxone or Cefuroxime, AND Doxycycline or Azithromycin

          (for atypicals the big three to know are:
          – Mycoplasma pneumoniae,
          – Legionella,
          – Chlamydia pneumoniae.
          – Others include, Chlamydia psittaci (psittacosis. Key word here is birds), Coxiella burnetti (Q fever. Key word here is cattle), Francisella tularensis (Tularemia. Key word here is rabbits))
Asthma Exacerbation

If you want a thorough review of asthma in primary care, head back to the Asthma episode https://thegenerehlist.ca/2020/12/20/ccfp-exam-key-topic-asthma/

An asthma exacerbation is defined as: acute or subacute episodes of progressively worsening shortness of breath, coughing, wheezing, and chest tightness.

In an acute exacerbation of asthma, the goal is for rapid reversal of airflow limitation and correction of hypoxemia and hypercapnia. 

  • Supplemental oxygen should be administered to patients who are hypoxemic with an SpO2 < 90% with a target of SpO2 > 92%
  • Short-acting beta-2-selective agonists (SABAs) are the mainstay of treatment of acute asthma exacerbations.
    A commonly used agent is albuterol, otherwise known as Salbutamol. Typically, this is administered three times in the first hour. Administration via metered dose inhaler (MDI) with a spacer device is as effective as nebulizer, unless of course they won’t be able to coordinate their inhalation. 
  • Inhaled ipratropium, which is a short-acting inhaled anticholinergic, is added to cases of moderate or severe asthma exacerbation.
    • The dosing is 500 mcg by nebulizer or 4-8 puffs by MDI every 20 minutes for the first hour and then PRN for up to 3 hours.
  • Early administration of systemic glucocorticoids is recommended for patients who do not have a sustained improvement in symptoms and PEF after initial SABA and anticholinergic therapy.
    • Typically, the equivalent of prednisone 40-60 mg (1 mg/kg/day) in a single or divided dose is given within the first hour.
    • There is no difference in results when comparing oral vs IV glucocorticoids. Note that it can often take up to 6 hours for the onset of action of systemic glucocorticoids to become clinically evident.
  • Administration of a single dose of IV magnesium sulfate is suggested for patients with severe asthma exacerbation unresponsive to initial therapy as it can act as a bronchodilator in acute asthma.
    • This is administered as IV magnesium 2 grams infused over 20 minutes.

It’s important to note that asthmatics can decompensate very quickly so equipment and personnel for rapid sequence intubation should also be readily at hand in case it is needed.

Disposition:
After initial stabilization, the question remains of whether your patient can now go home or if they require admission into hospital. This is largely guided by clinical judgement including the patient’s response to therapy, symptomatic status, airflow limitation, outpatient supports, as well as the patient’s history of asthma control and severity of past exacerbations. Each patient requires an individualized assessment. 

However, a general approach is as follows:

  • After the first hour of treatment, a patient whose symptoms have resolved and PEF is >80% can be discharged home safely.
  • If a patient has had an incomplete response and their PEF remains between 60-80%, they must be observed for another 1-3 hours and reassessed after that time.
  • If following those 1-3 hours, the patient has not shown significant improvement or their PEF remains unchanged, they will need to be observed overnight in the Emergency Department or admitted to hospital.
Acute heart failure (in old terminology CHF exacerbation)

Acute heart failure is defined as new or worsening symptoms and signs of heart failure. It can be de novo (⅓ of patients) or an an exacerbation of previously known heart failure (acute decompensated heart failure)

Triggers: 

You can use the mnemonic FAILURES to remember the common precipitants of acute heart failure

  • F – Forgetting medications or taking drugs that can worsen HF (e.g. BB, CCB, NSAID), chemo (anthracyclines, trastuzumab), toxins
  • A – Arrhythmia – especially atrial fibrillation
  • I – Ischemia or infarction; myocarditis, acute valvular dysfunction
  • L – Lifestyle choice: Dietary indiscretions – high salt, alcohol, excessive fluid intake
  • U – Upregulation – For example pregnancy and hyperthyroidism
  • R – Renal failure – acute, progression of CKD, or insufficient dialysis → increase in preload
  • E – Embolus (pulmonary) or COPD – lead to increase in afterload (n.b. COPD must be severe enough to cause cor pulmonale)
  • S – Stenosis (worsening aortic stenosis or renal artery stenosis) leading to hypertensive crisis. Hypertensive crisis leads to increased LV afterload. 

*Infection or anemia may also cause exacerbations

Diagnosis
Acute heart failure is a clinical diagnosis based on at least one of the following symptoms: 

  • Exertional dyspnoea
  • Fatigue
  • Paroxysmal nocturnal dyspnea (sensation of SOB that awakens patient, often after 1-2 hours of sleep) and is usually relieved in the upright position.
  • Orthopnea (Sensation of breathlessness in the recumbent position relieved by sitting or standing)
  • Cough
  • Early satiety
  • Weight gain
  • Increasing abdominal girth

On exam you may find the following: 

  • Positive abdominojugular test “Hepatojugular Reflux” – LR 8.0
  • Apical impulse lateral to MCL when supine: LR 5.8
  • HR > 100 bpm at rest: LR 5.5
  • S3 gallop – LR 3.9
  • Jugular venous distention – LR 3.9
  • Bibasilar crackles, though not helpful differentiating from COPD
  • Abdominal distention, due to ascites
  • Hepatomegaly
  • Peripheral edema

Your initial workup should include:

  • CBC-diff
  • Complete metabolic panel 
  • (CCS recommends Cr, BUN, glucose, sodium, potassium, troponin) 
  • BNP (minimal evidence for serial BNP measurements. If you trend BNP or troponin I will judge you)
  • +/- LFTs (if suspecting congestive hepatopathy), ABG (if they’re in severe respiratory distress)
  • 12 lead ECG
  • CXR
  • TTE (if no previous study)

Treatment 
A common mnemonic is LMNOP, but I urge you to erase it from you memory as morphine is associated with significantly increased mortality in patients with acute heart failure (OR 4.84)

In hospital/urgent care

  • Monitor O2 saturations, vital signs, and cardiac rhythm
  • Oxygenation – Target O2 sats > 90% with non-invasive ventilation as needed. 
  • Diuresis – IV furosemide 20-80mg bolus (depending on degree of fluid overload and home dose of furosemide). Furosemide infusions can be used, but there is no evidence of superiority. 

*IV furosemide is twice as strong as PO. E.g. 20 mg IV = 40 mg PO.

Sarah generally doubles their home dose, so if they were on 40 mg PO QD at home, I would give 40 mg IV daily to start

*Insert a foley! Heart failure patients are often elderly, frail, and at high risk of falling. Multiple nighttime bathroom visits are an avoidable danger*

  • Nitrates – Consider nitrate use if initial response to diuretics is not sufficient to alleviate respiratory distress. 

*Consult cardiology if patient is acutely unstable with refractory hypotension or high oxygen needs

In clinic: 

  • Refer to a Heart Failure Clinic if your patient has recurrent HF hospitalizations (CCS)
  • Send patient for ED assessment if they are hypotensive, hypoxic, or may require IV furosemide (e.g early satiety/significant weight gain are signs that their intestines are likely edematous and will not absorb PO furosemide)
Objective Two:
Regularly reassess adherence (compliance) to the treatment plan (including medications)

Successfully doing this requires a trusting relationship where your patient feels comfortable being honest with you about whether or not they have been actively performing the agreed-to therapies. These might be lifestyle changes, activity levels or medications. 

An element to consider when reassessing is considering if you are thinking in terms of ‘patient adherence’, as opposed to viewing it as barriers the patient is facing in trying to carry out the recommended therapies.

This is important because it can save you from advancing treatments or new interventions assuming the previous measure wasn’t working, when it was only because the measures just weren’t entirely implemented.

There are a number of tips to help overcome some patient’s barriers to carrying out the recommended therapies that we will cover more fully in objective five.

Objective Three:
In patients with chronic disease 
a) Actively inquire about pain.
b) Treat appropriately by: titrating medication to the patient’s pain, taking into account other treatments and conditions, considering non-pharmacologic treatment and adjuvant therapies

You should be seeing your patients with chronic disease on a regular basis, to check in and track any progression, improvements, or adjunctive difficulties such as social, mental health, functional inquiry and any pain.

To enable the best management of their pain, you need to do a full inquiry. OLD CARTS or whichever system you use to be thorough each time. 

You want to elucidate what type of pain you are dealing with: nociceptive, inflammatory, neuropathic, or possibly nociplastic or central sensitization pain.

Doing so will ensure the most appropriate approach. 

We don’t want to totally forego this objective, but I think we covered this reasonably well in Objective four of the Chronic Pain episode https://thegenerehlist.ca/2021/05/16/ccfp-key-topic-chronic-pain/

This goes through the process of treating Chronic pain including non-opioid pharmacologics, non-pharmacologic options, and even some nuance around initiating, titrating and weaning of opioids. Re-linking to this document will be here in the show notes https://tools.cep.health/tool/management-of-chronic-non-cancer-pain/

Regarding Neuropathic Pain:

There is a brand spanking new smiley face tool published in the May 2021 Canadian Family Physician following a systematic review for Neuropathic pain:

Objective Four:
Patients with chronic disease, actively inquire about: the psychological impact of diagnosis and treatment, functional impairment, underlying depression or risk of suicide or underlying substance abuse.

Receiving a diagnosis of chronic disease, particularly if the prognosis is life-shortening can be a major shock to your patient. Ensure you set sufficient time for your patient to absorb what you have told them at diagnosis and that they know you are available to answer any questions that might come up in future visits if needed.

In addition to the diagnosis, starting of treatment, such as chronic puffer use, or insulin as examples, can be a dramatic change to their life, and can also sometimes be quite stigmatizing still. You can help by asking them how they are feeling about the treatments and if there is any way you can help to make it easier on them to take their medications or other therapies.

Functional Impairment

Good old ADLs and iADLS, ADLs usually referring to things within the home, and iADLs referring to things outside the home. 

if you need a reminder to prompt this in the heat of the moment, remember DEATH SHAFT

  • Dressing
  • Eating, or feeding self
  • Ambulation, asking if they need a walker or if they hold walls when walking or transferring
  • Toiletting, including wiping sufficiently
  • Hygeine, ability to bathe or shower self, brush teeth, etc
  • Shopping
  • Housekeeping or housework
  • Accounting or managing money
  • Food preparation
  • Telephone use and transportation
underlying depression or risk of suicide or underlying substance abuse.

Just because they have a chronic disease does not change how you screen for depression, but it should be a prompt that you screen at all. So use your PHQ-2 and SIGECAPS.

None of the screens for suicide risk are validated, as far as my research can find. However, you should still have frank conversations with your patients who have chronic disease about whether or not they have had thoughts of harming themselves or others.

Regarding substance use screening, there will be an entire episode dedicated to this, so keep your eyes peeled.

Objective Five:
Given a non-compliant patient, explore the reasons why, with a view to improving future adherence to the treatment plan.

Again, this wording should probably give you a bit of a visceral reaction. Reframing from ‘non-compliant’ patients, instead looking to barriers preventing them from carrying out the recommended interventions is likely going to be more helpful.

Remain objective and non-confrontational to allow for honest feedback from the patient as to what they feel are the barriers to them carrying out the recommended therapies.

A national survey by the Canadian Pharmacist Association in 2015 found that 30% reported stopping their medications before they were advised to, and a quarter didn’t fill the prescription at all. The survey attempted to explore the reasons given by patients for not taking their medications as prescribed and the most common reasons given were:

  • For the 25% who didn’t fill the rx at all, 
    • 20% said it was because their insurance didn’t cover enough of the cost
    • 12% said they didn’t have insurance and so could not afford it
  • For the 30% who stopped before they were advised to:
    • 45% felt they didn’t require it any more
    • 18% said it made them sick and they didn’t think it was helping
    • 8% said they couldn’t afford to keep taking it

Failure to Take Meds Leads to Worsening Health Outcomes and Increased Costs to Health Care – English

While this is specific to antihypertensives and with low grade evidence, hypertension canada in their 2020 guideline updates suggest using a multi-pronged approach using a few tips including:

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