Diabetes

Question 1

Diabetes leads to physiological ____

Answer 1

aging

• Pt with T1DM who has poor contorl of BG ages approximately 1.75 years physiologically for everychronoclogic year of dx.
  
  • If good control BG, age 1.25 years
• T2DM age 1.5 years (with poor control) and age 1.06 years with tight control BG and BP

Question 2

Type 1 vs Type 2 DM?

Answer 2

• Type 1
  
  • commonly due to T cell mediated autoimmune destruction of the beta cells
  • usually younger, 15% prevalence of other autoimmune dx (graves, hasimoto, addison, MG)
    
    • typically not obese
  • presents with an absolute insulin deficiency- need exogenous insulin
  • concordance rate of 40-50% in twins
  • susceptible to DKA if insulin held
    
    • ​more labile in BG and more episodes of hypoglycemia
  • increase in insulin in post midnight hours (dawn phenonmenon) from nocturnal surge in GH causes increase in BG upon awakening.
• Type 2
  
  • due to progressive reduction in insulin secretion by the beta cells; coupled with insulin resistance at the tissue level
    
    • normal to high levels of insulin with relatively low levels of insulin for the corresponding hyperglycemia.
    • hyperinsulinemia is postulated to cause accerleated CV dx
  • concordance rate 100% in twins
  • not susceptible to DKA if insulin held
    
    • ​fewer BG fluctuations and may reach hyperosmolar state at high BG levels
  • susceptible to development of HHNK (hyperglycemic-hyperosmolar nonketotic state)
  • Long term, strict contorl BG and BP, regular physical activity, delays onset of microvascular complications
  • can be on carabose, meglitinide, metformin, sulfonylureas, thiazolidinediones, DPP IV inhibitors to help with BG control

italicized= Oguin notes from ppt slides

Question 3

What is gestational diabetes?

Answer 3

• >3% of all pregnancies
• increases the risk fo t2DM by 17-63% within 15 years

Question 4

Why do we care about intraoperative glycemic control?

Answer 4

prevents complications

• Anesthetic consequence of long standign hyperglycemia are similar
• neuroendocrine responses during periop period restuls in an increase in the level of catecholamines and stress hormones resulting in hyperglycemia
• hypoglycemia is more detrimental

Question 5

What is glucotoxicity? What are some of glucotoxicity’s consequences?

Answer 5

Glucotoxicity is non-enzymatic glycosylation reactions

1. leads to formation of abnormal proteins which:
   
   • weakend endothelial junction and decrease elastane
   • decrease wound healing tensile strength
2. increased macroglobulin production by the liver
   
   • leads to increased blood viscosity
   • promotes intracelleluar swelling by facoring the production of nondiffiusible, large molecules (sorbitol)
3. Disrupts autoregulation:
   
   • glucose induced vasodilation prevents target organs from protecting against increase in systemic blood pressure (prevents vasodilation)–> end organ damage
   • high glucose concentration impair endothelial function by suppressing formation of ntric oxide and impairing endothelium dependent flow- mediated dilation and abnormaliites in hemostasis (increased PLT activation, adhesion, aggregation, reduces fibrinolytic activity)
     
     • ​negative effects in patient with ACS; also limits ability of cardiac muscle to uptake glucose for anaerboic metabolism (can’t compensate as well)
4. leads to osmotic diuresis –>
   
   1. consequent hypovolemia
   2. prerenal azotemia
5. Immunity dysfunction
   
   1. impairs leukocyte funciton
   2. decreased phagocytosis
   3. impaired bacterial killing and chemotaxis
      
      • Hyperglycemia results in nuclear factor kB activaiton and production of inflammatory cytokines such as TNF-a, IL-6 and plasminogen activate inhibitor 1
        
        • ​causes increased vasuclar permeability and plt activation

Question 6

Diagnostic criteria for DM?

Answer 6

• Fasting plasma glucose of 126 mg/dL or greater
• 2 hours plasma glucose of 200 mg/dL or greater after oral GTT
• HBA1C >6.5%
  
  • can give idea of autonomic dysfunction
• Random plasma glucose of 200 mg/dL or greater in pt with classic symptoms of hyperglycemia and hyperglycemia crisis
• 45.8% of all cases of diabetes are undiagnosed

Question 7

Non diabetic hyperglycemia pathophys?

Answer 7

• 40-60% of patients without hx of diabetes experience transient hyperglycemia due to stress of surgery
• stress hormones and cytokines, and the CNS interfere with insulin secreiton and action
• result: increased hepatic gluocse produciton and reduced glucose uptake in peripheral tissues
  
  • leads to inflammatory and oxidative stress
• maintenance of normolgycemia is essential to maintain physiologcy
  
  • ​short periods of increased BG lead to inflammation and oxidative stress even in non diabetics
    
    • ​pt without dm have worse outcomes with hyperglycemia c/t patients with previous hx diabetes! (no compensatory mechanism)
    • stress hyperglycemia in pt without DM undergoing sx has
      
      • 4 fold increase in complications and
      • 2 fold increase in death c/t pt with normoglycemia and to subjects with DM. _TLDR- Non diabetics have worse outcomes with periop hyperglycemia_

PIC:

• Surgical stress causes increased catecholamines, glucagon, cortisol, GH which signals adipose to start lipolysis and pancreas to reduce insulin prduction (this increases FFA availability to liver). also causes liver to gluconeogenesis, gycogenolysis and glucose output.
• both decreased insulin and increase glucose causes hyperglycemia
• hyperglycemia–>
  
  • mitochondrial injury
  • endothelial dysfunction
  • immune dysregulation
    
    • increase cytokines TNF-a, IL-6 and IL-1–> increased insulin resistance by interfering with insulin signaling
  • superoxide generation

Question 8

What is metabolic syndrome? Diagnostic features?

Answer 8

• Insulin resistance syndrome with:
  
  • HTN
  • dyslipidemia
  • procoagulant state
  • obesity
• Significance:
  
  • associated with premature atherosclerosis
  • high risk of developing DM
  • Affects 25% of US population
• concurrent dx with DM

Diagnostic features OF METABOLIC SYNDROME: ( if > 3 of following–> metabolic sydnrome)

• fasting plasma glucose >110 mg/dL
• abdominal obesity
  
  • waist girth >40” men
  • >35” women
• serum triglyercisde level >150 mg/dL
• serum HDL :
  
  • <40 mg/dL in men
  • <50 mg/dL in women
• Blood pressure >130/85

Question 9

What are some goals for DM treatment?

Answer 9

• goal of treating DM is not just to contorl glucose levels, but also keep:
  
  • HBAC <7%
  • LDL <100 mg/dL;
  • HDL >40 mg/dL in men and >50mg/dL in women
  • TG <200 mg/dL
  • BP <130/80

Question 10

What are some major surgical risk factors with diabetes?

Answer 10

• Intraop glycemic contorl is critical to preventing complications
• major sx risk factors: end organ diseases associated with dm:
  
  • CV dysfunction
  • renal insufficiency
  • joint collagen tissue abnormalities (limitaiton in neck extension, poor round healing),
  • inadequate granulocyte production
  • neuropathies (issues with regional)
• • poor preop glucose control (elevated HBA1C)= independent predictor of worse periop outcomes
    
    • anesthetic consequences of long-standing hyperglycemia similar for type 1 and 2
    • neuroendocrine resposne during periop period results in increase in level of catecholamines and stress hormones leading to hyperglycemia
• major focus of perop eval is treatment of these dieseases to ensure optimal preop conditions

Question 11

What are some various ways that surgery impacts diabetes and BG?

Answer 11

1. Neuroendocrine stress response to srugery causes release of counterregulatory homrons:
   
   • glucagon, epinephrine and cortisol:
     
     • leads to:
       
       • inhibits insulin secretion
       • increased insulin resistance
       • mobilization fo glycogen
       • increased gluconeogeneis
2. The severity of insulin resistance and hyperglycemia are directly related to degree of surgical trauma. Increased incidence following:
   
   1. cardiac sx
   2. major abdominal sx
   3. procedures of long duration
   4. open procedures >than laparoscopic procedures
3. Inhaled anesthetics contribute to periop hyperglycemia by depressing insulin secretion in response to increasing BG levels
4. periop steroid admin further exacerbates the propensity toward hyperglycemia
   
   • iatrogenic hyperglycemia is also a factor– d/c of oral meds and insulin contribute to periop hyperglycemia
   • single dose decadron- doesn’t have delitirous effect on wound healing or pt outcome

Question 12

Therapy classes of oral antidiabetic meds? MOA?

secretagogues?

incretins?

DPP-4 inhbitors?

Biguanides?

TZD?

Alpha-glucosidase inhibitors?

Answer 12

• Secretagogues (sulfonylureas (glyburide, glipizide) & meglitinides (glinides))
  
  • increase insulin availability–> hypoglycemia
  • controversial in CV disease- may have harmful CV effects
  • first DOC in lean, insulinopenic pt
• Incretins (exanatide [BYetta] and liraglutide)
  
  • increase glucose-stimulated insulins secretion–> hypoglycemia
  • suppress glucagon
  • slow gastric emptying–> risk for aspiration
• Dipeptidyl peptidase- 4 inhibitors (saxagliptin, sitagliptin, vildagliptin)
  
  • inhibit the degradation of native GLP-1 na dnehance glucose-stimulated insulin secretion
• Biguanides (metformin)
  
  • suppress excessive hepatic glucose release
  • obese, insulin resistant- prefer biguanides
• Thiazolidinediones or glitazones (rosiglitaxone, pioglitazone)
  
  • improve insulin sensitivity
  • if insulin resistant with renal impairment–> glitazones
• alpha-glucosidase inhibitors (acarbose, miglitol)
  
  • delay GI glucose absorption

Question 13

Oral drug therapy and surgery considerations?

Answer 13

• Metformin is commonly held on DOS d/t risk for lactic acidosis
  
  • evidence is not strong
  • risk highest in pt with renal insufficiency
• SUlfonylureas {glyburide, glipizide] and glinides (aka meglitinides) increase intrinsic insulin production and confer r/f periop hypoglycemia–> stopped periop
• Incretins have sig. GI S/E (n/v, delayed gastric emptying) esp during initiation of txmt (4-8 weeks) (incretins include DPP-4 inhibitors- xJanuvia, byetta and symlim)
  
  • don’t worry about hypoglycemia but worry about risk for aspiraiton at induction
  • no deep extubation

Question 14

General rule for antihyperglycemia agents and use DOS?

Answer 14

• Skip most except DPP-4 inhibitors (continue regular use and consider aspiration precautions)
• Long acting basal insulin- take 50% of dose
• mixed insulin (combo long/short)-
  
  • if morning BG >200, take 50% of dose
  • If <200, skip AM dose

Question 15

Injectable insulin around surgery?

Answer 15

• Type 1 diabetics are insulin dependent
  
  • need insulin even when fasting–> otherwise ketosis
• Approximately 50% of basal requirements of insulin in type 1 diabtics used to cover metabolic demands without inducing hypoglycemia
  
  • T1DM need insulin even while fasting to prevent ketosis
• Long acting insulins do not peak and confer less risk of hypoglycemia introp
• short acting insulin is typically held DOS
  
  • 1/2 the dose can be given in am if bg >200
  • if BG <200; do not give short acting insulin morning of sx

***** Oguin will test over insulin table on picture******

Question 16

Preop eval of daibetics?

Answer 16

• Diabetic hx- type, duraiton
• note pharmacologic anti-hyperglycemic regiman
  
  • develoip plan for periop period
  • insulin pumps will require special attention and didscussion- coordinate with PACU
• Discuss occurrence and frequency of hypoglycemia if present
• document and evaluate microvascular and macrovascular complications from diabetes
  
  • focus: CV, renal, neuro, MS
• Document current BG;and note the self reproted “average” of BG
• Evaluate hydration status (osmolar diuretic effect with hyperglycemia; renal disease)
• Diabetic patients (especially those taking insulin) are best done as first case of the day
• don’t keep NPO too long!!!

Question 17

How do you treat hyperglycemia dos?

Estimated decrease in BG?

Answer 17

• Give 1-4 units of insulin per 50 mg/dL decrease in glucose desired
• IV vs SQ- IV preferred
  
  • unpredicatble SQ abroption of insulin with edema, hypotension and peripheral vasoconstriction
  • surgeries with large fluid shifts or hemodynamic lability: skin perfusion can affect SQ absorption
• IV insulin admin can adhere to IV tubing

Question 18

What can periop hyperglycemia cause?

Answer 18

• Immune function inhibited
• prothrombotic state promoted
• fluid and electolye imbalances accompnay glycosuria
• pre-existing gastroparesis and pulmonary dysfunction are worsened by hyperglycemia
• pulmonary complications are more frequent in pts with poorly contorlled T1DM
• Glycosuria beings at blood glucose of 180 mg/dL causing fluid shifts, dehydraiton and electolyte abnormalities

Question 19

When do we cancel sx in diabetics?

Answer 19

• No clear guidliens; many cancel elevtive cases for BG >350 mg/dL
  
  • elective cases are certianly cancelled in pt with DKA/HHNK
• Note: pt with high glucose on DOS have osmotic diuresis-induced hypovolemia
• Emergent cases are done irrespective of blood glucose
  
  • ONLY MOST urgent cases can proceed if pt is in active DKA/HHNK
• Elective case and previously indiagnosed?
  
  • ADA does not recommend HbA1c threshold above which elective sx should be postponed
  • takes 3 months to show improvmeent after pharmcaological and non-pharmacological treatment is started

Question 20

Inuslin pump management during sx?

Answer 20

• Typical recommendation: maintain the basal dose during the preoperative fasting period
  
  • Consider reducing the dose by 10% to 20% to prevent hypoglycemia
  • <1 hour (case length) can keep pump running
  • 1-3 hours disconnect pump with plan to resume in PACU
• Emergency procedures and procedures >3 hours
  
  • Disconnect insulin pump and start an infusion titrated to glycemic control goal
• Endocrine consult recommended for recommendations on peri-operative management in patients who are labile
• if pt going to have MRI or need potnetial defib during procedure–> must stop pump
• if mental status quesitonable–> stop pump
• if insulin infustion–> chekc q 30 min because no s/s hypoglycemia under anesthesia

Question 21

Guidelines for BG managmeent of pt with insulin pump? What is target BG if pt on insulin gtt during procedure?

Answer 21

target BG 140-180 mg/dL for pt needing insulin infusion

see chart in picture for considerations of short, intermediate and long procedures

• Short <1 hour
  
  • may keep pump connected
  • if preop BG >300, consider using insulin infusion
• Intermediate (1-3 hours)
  
  • if BG in target range, ask pt to admin bolus equivalent to insulin pump basal rate/1 hr. hold bolus if BG <110
  • IF BG above target, ask pt to treat in usual fashion
  • disconnect pump and keep outside procedure room
  • if preop BG >300–> Insulin infusion
• Long (>3 hours)
  
  • DC insulin pump
  • give to family member
  • begin IV insulin infusion
    
    • if basal <1 unit/hr–> 0.5 unit/hr
    • if basal >1 unit–> start IV insulin 2/3 normal rate
  • maintain BG 140-180 (get postop endocrine consultation)
    
    • patient may resume insulin pump postop when cognitively alert

Question 22

Intraop BG goal? mix for insuiln gtt? rate?

What sx/conditions do you have higher insulin requirements?

How often do you check BG?

Answer 22

• Intraop goal 120-180 mg/dL
  
  • >200 mg/dL: glycosuria;dehydration; inhiibited wound healing
• Typically 1 unit of insulin lowers glucose approcimately 25-50 mg/dL
• Insulin drip ~0.02 unit/kg/hr
  
  • mix: 100 units regular insulin in 100 mL of normal saline (1unit/mL)
  • concurrent infusion of D5%1/2 NS with 20 mEq KCl at 100-150 mL/hr
    
    • need to infusion of carbs to inhibit hepatic glucose produciton and protein catabolism
• Higher insulin infusion requirements:
  
  • CABG
  • STEROID admin
  • severe infection
  • TPN
  • vasopressor
• Check glucose q 30 min–>1 hours
  
  • typically want venous samples because BG runs higher

Question 23

What is DKA? diagnosis?

Answer 23

• Blood ketoacid concentraiton is elevated form increased lipolysis of fat and subsequent conversion of fatty acids to ketoacids
• more common in T1DM (DKA is frequently their 1st clinical presentation)
  
  • incidence of cardiac arrhythmias and hypotension from ketoacidosis are decreased when intravascular volume depletion and hypokalemia are at least partially treated
• Diagnosis:
  
  • ​Glucose >250 mg/dL
  • Acidosis
    
    • pH <7.3
    • HCO3 18 mEq/L
    • Anion gap >10
  • Positive urine/serum ketons
• Emergency sx:
  
  • delay of case may worsen metabolic derangement (ruptured appendix, ichemic bowel
  • attempt to at least intiitate correction of volume depletion and hypokalemia before sx when feasible
    
    • give fluids, corect K –>

Question 24

What do we start insulin drip at in DKA? Drop in BG?

Electrolyte/fluid balance effects of DKA?

Answer 24

• Initial treatment: 10 units IV insulin (vs. 0.1units/kg) followed by continuous infusion (0.1units/kg/hr)
  
  • Maximum rate of decline in glucose is fairly constant and averages 75 to 100 mg/dL/hour, regardless of the dose of insulin
  • When glucose reaches 250mg/dL D5 should be added to the maintenance fluid
• PROFOUND HYPOVOLEMIA: Fluid deficits can be substantial- 3 to 5L and up to 10L
  
  • Deficit is corrected slowly: 1/3 estimated deficit corrected in first 6-8 hours and remaining 2/3 corrected over next 24 hours
  • Must monitor LV function with fluid resuscitation if hx of CV dysfunction
  • Sodium must be corrected concurrently (use normal saline)
• Hypokalemia must be treated with DKA- potassium levels drop precipitously once insulin infusion is started
• Hypophosphatemia can lead to diaphragmatic and skeletal muscle dysfunction and impaired myocardial contractility
• Critical to follow glucose, potassium, and arterial pH; watch also Mg++ level and replace PRN

Question 25

What is hyperglycemic hyperosmolar syndrome?

Answer 25

• Type 2 diabetics
  
  • Usually concurrent acute illness
  • >60 yo more vulnerable
• Severe hyperglycemia, hyperosmolarity, and dehydration
• Metabolic acidosis (without ketoacidosis)
• Sx:
  
  • polyuria
  • polydipsia
  • hypovolemia
  • hypotension
  • tachycardia,
  • organ hypoperfusion
  • mental obtundation at (>340 mOsm/L)
• Tx: fluid resuscitation, insulin administration, and electrolyte supplementation
  
  • may give hypotonic saline (1000-1500mL/hour) until OsM <320 mOsm/L and then isotonic saline (1000-1500mL/h) can be given
  • Insulin therapy is initiated with IV bolus of 15 units regular insulin followed by 0.1 unit/kg/hr infusion
  • Decrease insulin to 2-3 units/hr when the glucose level decreases to 250-300mg/dL
  • Electrolyte deficits are significant, but usually less severe than in DKA

Question 26

S/S hypoglycemia?

When might these s/s be impaired?

Answer 26

Symptoms:

• Adrenergic excess:
  
  • tachycardia
  • palpitations
  • tremulousness
  • diaphoresis
    
    • Repetitive episodes can lead to lack of autonomic symptoms “hypoglycemic unawareness”
• Neuroglycopenia:
  
  • headache,
  • confusion,
  • mental sluggishness,
  • seizures,
  • coma
• All symptoms may be masked by anesthesia
  
  • Can lead to irreversible neurological damage
  • Recognition also impaired with:
    
    • sedatives
    • analgesics
    • β-blockers
    • sympatholytics
    • Pt with autonomic neuropathy
• Poorly controlled type 2 diabetics can have hypoglycemic symptoms at normal glucose levels
• Requires frequent glucose monitoring
• Tx if LOC altered: glucose 0.5 g/kg IV or glucagon 0.5–1 mg IV, intramuscularly, or subcutaneously

Question 27

Treatment of hypoglycemia?

Answer 27

• Glucose 0.5 g/kg IV
• Glucagon 0.5-1 mg IV, IM or SQ

Treatment consists of admin 50 mL of 50% destrose in water, which typically increases the glucose level 100mg/dL or 2 mg/dL/mL

Question 28

Which type of diabetic is more likely to experience hypoglycemia? Why?

Answer 28

Type 1 Diabetic

• Type 1 diabetics have impaired release of counter-regulatory hormones, whereas type 2 patients do not
• type 2 pt rarely encounter hypoglycemia, even when using insulin
• Type 2 patients may experience s/s of hypoglycemia at normal blood glucose levels- so be cautious in glucose correction in these patients

Question 29

Considerations in diabetic airway?

Risk factors for predicting difficult airway in the diabetic?

Answer 29

• 1/3 long standing diabetics are difficult airways
• diabetic cheiroarthropathy
  
  • TMJ and cervical spine joints affected
  • accumulation of AGEs and abnormal cross-linking of collagen in joints
• Prayer sign is indicative of cheiroarthropathy
• Risk factors:
  
  • advanced age
  • female sex
  • long duration fo diabetes
  • poor glycemic control
  • presence of microvascular complications like neuropathy and retinopathy

Question 30

Connection betwen CAD and DM?

Answer 30

Coronary artery disease

• Diabetes induces a proatherogenic procoagulant state by:
  
  • inhibiting nitric oxide
  • production of reactive oxygen species
  • increasing receptors for AGE
  • impairing platelet function coupled with impaired fibrinolysis.
• Hypertension, hyperlipidemia, obesity, and uncontrolled BG lead to accelerated atherosclerosis in these patients
• Heart failure (systolic and diastolic) occurs more frequently than in non-diabetics
• Diabetes increases the risk of perioperative cardiac complications
• Elevated risk of painless “silent” MI with autonomic neuropathy
• Pre-operative cardiac assessment is imperative

Question 31

Connection between peripheral vascular disease and DM?

Answer 31

Peripheral vascular disease- MACROvascualr complication

• ~20% of diabetics have peripheral artery disease (PAD)
  
  • Suspect underlying coronary or cerebrovascular disease (CVD) with PAD
  • Adverse cardiac and cerebrovascular events are more pronounced in diabetic patients with PAD
  • Arterial access is very challenging with severe PAD
    
    • may need US to scan artery, see plaque, maybe need a brachial art line instead

Question 32

Connection between cerebrovascular dx and DM?

Answer 32

Cerebrovascular disease- MACROvascular dx

• Increased risk d/t:
  
  • Systemic inflammation
  • vascular smooth muscle dysfunction
  • endothelial dysfunction
• Increased risk of ischemic stroke even in young diabetic patients
• History of poor glucose control can lead to impaired cerebrovascular reactivity under anesthesia
• Intraoperative hyperglycemia may worsen the outcome of intraoperative neurologic insults
• If CVD or carotid stenosis suspected: maintain adequate perfusion pressures to decrease the risk of perioperative stroke

Question 33

What are some macrovascular complications of DM?

Answer 33

• Cardiovascular
• Peripheral Vascular
• Cerebrovascular

Question 34

What are some microvascular complications of DM?

Answer 34

• Retinopathy
• Nephropathy
• Autonomic neuropathy
• Peripheral neuropathy

Question 35

What is diabetic retinopathy? anesthesia considerations?

Answer 35

Diabetic Retinopathy- microvascular dx

• the most common microvascular complication of diabetes
  
  • may signal the presence of long-term nephropathy
• proliferative or nonproliferative (dont’ need to know difference)
  
  • proliferative: microangiopathy leads to capillary occlusion and retinal ischemia which increases the levels of vascular growth factors
• Multi-factorial vision loss: maculopathy, vitreous hemorrhage, detachment, or neovascular glaucoma
• Document pre-operative vision deficits
  
  • Most important in cases with risk of POVL (postop vision loss) (ex: spine surgery)

Question 36

Presentation of diabetic nephropathy? periop goal? strategies to reduce risk of AKI?

Answer 36

Diabetic Nephropathy- microvascular

• Presentation: htn, albuminuria, peripheral edema, and progressive reduction of renal function (GFR)
• Diabetes is a leading cause of ESRD in the US
• Diabetic patients are often treated ACE inhibitors, even in the absence of gross hypertension

Perioperative goal: reduce the risk of perioperative acute kidney injury (AKI)

• Perioperative strategies to reduce risk of AKI:
  
  • Maintaining euvolemia
  • Ensuring adequate renal perfusion
  • Avoidance of nephrotoxic medications (including aminoglycoside antibiotics)
    
    • NSAIDs: inhibit prostaglandins, impair renal blood flow, and worsen renal function
    • selective cyclooxygenase-2 inhibitors potentially have a similar effect on renal function as well

A combination of:

• diuretics (hypovolemia)
• NSAIDs- inhibition of prostacyclin synthesis leading to renal afferent arteriolar vasoconstriction
• and ACE’s/ ARB’s- reduction in GFR d/t efferent arteriolar vasodilation

​ are associated with an increased risk of AKI (Lapi, F, et al., BMJ 2013;346:e8525)

Question 37

What are some acid base and electrolyte imbalances in patients with renal nephropathy? What are some hematologic consequences?

Answer 37

Every system is affected when renal function is compromised:

• hyperkalemia
• metabolic acidosis from bicarbonate loss and retention of organic acids
• anemia from reduced erythropoietin production
• platelet dysfunction secondary to uremia
  
  • not quantitative but qualitative d/t uremia

Question 38

What is autonomic neuropathy ?

Answer 38

Autonomic Neuropathy- microvascular complication

• Primarily affects the cardiovascular and gastrointestinal systems
• Pre-op warning sx:
  
  • poor exercise tolerance
  • orthostatic blood pressure changes
  • early satiety
  • bloating
  • nocturnal diarrhea
  • erectile dysfunction
  • lack of sweating,
  • lack of pulse rate change with inspiration or orthostatic maneuvers
• Parasympathetic dysfunction precedes sympathetic dysfunction
  
  • Early small-fiber damage:
    
    • loss of vagally controlled normal HR variability,
    • decreased peripheral sympathetic tone
    • diminished sweating.

Sympathetic denervation: sympathetic nerves that supply small arterioles are absent or abnormally distant from their effector sites; damage to the vasa vasorum

• Baroreceptors in the carotid sinus and aortic arch are compromised
• Lower circulating norepinephrine levels in diabetics with orthostatic hypotension
• Presence of postural hypotension or gastroparesis =5-year mortality rates >50%

Question 39

Implications of autnomic neurpathy in diabetic patient?

Answer 39

• Potential for profound hypotension on induction due to poor vascular compensatory mechanisms
• Sudden cardiac deaths due to dysrhythmias have been reported in these patients
• If severe autonomic neuropathy is suspected:
  
  • Consider invasive blood pressure monitoring (A-line)
  • Potential postoperative intensive care unit admission for cardiac/ respiratory monitoring x 24-72 hours
  • Impaired respiratory responses to hypoxia; increased response to drugs that have depressant effects
  • Changes in heart rate normally seen with atropine or b-adrenergic blockers can be blunted (Hyman, 2013)

Question 40

How can we test for autonomic dysfunction?

Answer 40

• Panel of 5 tests of CV function developed to evaluate atunomic function
  
  • HR response to
    
    • valsava maneuver
    • standing up
    • deep breathing
  • blood pressure response to
    
    • standing up
    • sustained handgrip
• Tests involving changes ot HR measure parasympathetic system (these changes occur first)
• Tests involving changes in measures of BP reflect sympathetic injury

A positive result occurs when:

• Early involvement--single abnormal or two borderline abnormal results on the test involving changes in HR
• Definite involvement–- results abnormal on two of the tests of changes in HR
• Severe dysfunction- when abnormality in BP assessment

Question 41

GI manifestations of autonomic neuropathy and precuations taken in anesthesia?

Answer 41

Autonomic Neuropathy: Gastrointestinal manifestations

• gastoparesis sx: nausea, vomiting, bloating, early satiety
• Take precautions to reduce the risk of aspiration on induction
  
  • pro-kinetic agents and H2 antagonists and/or proton pump inhibitors
  • severe cases of gastroparesis: awake intubation in a semi-sitting position versus intubation after induction of anesthesia with RSI and cricoid pressure
    
    • the safest way if severe!!!

Question 42

Peripheral neuropathy in DM?

Answer 42

• Distal symmetric polyneuropathy (DSPN) is most common: ~75% of diabetic neuropathies
  
  • microvascular damage to the vasa nervosum and oxidative and inflammatory damage due to hyperglycemia
  • primary cause for diabetic foot ulceration and Charcot arthropathy (nonunion in footbone)
• Occurence:
  
  • 20% of patients with type 1 DM after 20 years of disease
  • 10% to 15% of patients with type 2 diabetes
• Initially: small sensory fibers are involved
  
  • paresthesias and neuropathic pain
• Later: larger fibers are involved
  
  • painless paresthesias and loss of protective sensations
  • insensate patients are higher risk of positioning injury

Question 43

Anesthesia consideration with peripheral neuropathy in diabetics?

Answer 43

• In a diabetic neuropathic foot: pain and temperature are lost before touch or vibration is affected
• Caution with positioning patients with diabetic neuropathy, especially if they are insensate, to avoid causing pressure injuries or ulcerations to the extremities

Regional anesthesia in patients with diabetic neuropathy:

• ultrasound- guided techniques may be favored in these patientsSave
  
  • electric stimulation threshold is increased
  • increased risk of stimulator needle trauma
• Diabetic nerves are more sensitive to local anesthetics and result in prolonged block duration
• There is an increase in the incidence of infection when nerve catheters are used for postoperative pain in patients with diabetes
  
  • do SS instead

Question 44

Postop complications DM?

Answer 44

• Higher rates of SSI’s
• Increased LOS and mortality after non-cardiac surgery
• Neuroendocrine stress response increases risk of hyperglycemia
• Goal (poorly defined): glucose 140-180 mg/dL in critically ill patients
  
  • insulin treatment for glucose >180 mg/dL

Question 45

Cuases of hypoglycemia in the non diabetic?

Answer 45

• Rare to see hypoglycemia in non-diabetic patients
• Causes: (all of these are extremely rare)
  
  • pancreatic islet cell cancer
  • large hepatoma
  • large sarcoma
  • alcohol ingestion
  • use of β-adrenergic receptor blocking drugs, haloperidol therapy,
  • hypopituitarism,
  • adrenal insufficiency,
  • altered physiology after gastric or gastric bypass surgery,
  • hereditary fructose intolerance,
  • ingestion of antidiabetic drugs,
  • galactosemia, or autoimmune hypoglycemia

Most common cause:

• Insulinoma: manipulation of the tumor will cause massive insulin release; intraoperative octreotide is used (suppresses insulin release)
  
  • typically only operated on at centers that can operate a mechnical pancreas

All symptoms of hypoglycemia are masked by anesthesia