diabetic ketoacidosis ppt
DESCRIPTION
TRANSCRIPT
A 55 year male patient was brought by relatives to the ESR with co pain and swelling over lt foot extending upto below kneePt also co abdominal pain and drowsiness since two days
OE- P120 bpm BP-10060 mmHg RR-30cpm Per abdomen exam reveals tenderness
General and systemic including airway exam
Routine blood investigations Hb10gm CBC 20200cumm RFTs amp
LFTs WNL RBS 320mgdl Serum electrolytes- Sr Na130mEql
Sr K 5mEql Chest Xray increased BVM ECG NSR
Urine routine microscopy
Special investigations Serum and urine ketones ++ ABG- pH725 pO290 pCO228 Sr
bicarbonate15 BE-9 SO297If a classic triad of DKA ie hyperglycemia
ketonemia and metabolic acidosis is seendiagnosis
A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia dehydration and acidosis-producing derangements in intermediary metabolism including production of serum acetone
Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin
deficiencydependence The presenting symptom for ~ 25
of Type I Diabetics
Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin
Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation
Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations
respiratory distress Abdominal tenderness (may resemble
acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema
possibly coma
INSULIN Administer short-acting insulin IV (01
unitskg) or IM (03 unitskg) then 01 unitskg per hour by
continuous IV infusion Increase 2- to3-fold if no response by 2ndash
4 h If initial serum potassium is lt 33
meqlcorrect K level while giving insulin to prevent dangerous hypokalemia
Expected fall is 50-100 mgh Transition into SQ when
A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO
FLUID1 Deficit is around 6-8 L ndash need NOT to
replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over
first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash
300mLh Change to 5 glucose and 045 saline
at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)
Watch BP pulse BUNcreatinine and urinary output
Use plasma expandersblood if in shock and does not respond quickly to saline
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
General and systemic including airway exam
Routine blood investigations Hb10gm CBC 20200cumm RFTs amp
LFTs WNL RBS 320mgdl Serum electrolytes- Sr Na130mEql
Sr K 5mEql Chest Xray increased BVM ECG NSR
Urine routine microscopy
Special investigations Serum and urine ketones ++ ABG- pH725 pO290 pCO228 Sr
bicarbonate15 BE-9 SO297If a classic triad of DKA ie hyperglycemia
ketonemia and metabolic acidosis is seendiagnosis
A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia dehydration and acidosis-producing derangements in intermediary metabolism including production of serum acetone
Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin
deficiencydependence The presenting symptom for ~ 25
of Type I Diabetics
Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin
Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation
Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations
respiratory distress Abdominal tenderness (may resemble
acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema
possibly coma
INSULIN Administer short-acting insulin IV (01
unitskg) or IM (03 unitskg) then 01 unitskg per hour by
continuous IV infusion Increase 2- to3-fold if no response by 2ndash
4 h If initial serum potassium is lt 33
meqlcorrect K level while giving insulin to prevent dangerous hypokalemia
Expected fall is 50-100 mgh Transition into SQ when
A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO
FLUID1 Deficit is around 6-8 L ndash need NOT to
replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over
first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash
300mLh Change to 5 glucose and 045 saline
at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)
Watch BP pulse BUNcreatinine and urinary output
Use plasma expandersblood if in shock and does not respond quickly to saline
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Special investigations Serum and urine ketones ++ ABG- pH725 pO290 pCO228 Sr
bicarbonate15 BE-9 SO297If a classic triad of DKA ie hyperglycemia
ketonemia and metabolic acidosis is seendiagnosis
A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia dehydration and acidosis-producing derangements in intermediary metabolism including production of serum acetone
Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin
deficiencydependence The presenting symptom for ~ 25
of Type I Diabetics
Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin
Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation
Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations
respiratory distress Abdominal tenderness (may resemble
acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema
possibly coma
INSULIN Administer short-acting insulin IV (01
unitskg) or IM (03 unitskg) then 01 unitskg per hour by
continuous IV infusion Increase 2- to3-fold if no response by 2ndash
4 h If initial serum potassium is lt 33
meqlcorrect K level while giving insulin to prevent dangerous hypokalemia
Expected fall is 50-100 mgh Transition into SQ when
A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO
FLUID1 Deficit is around 6-8 L ndash need NOT to
replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over
first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash
300mLh Change to 5 glucose and 045 saline
at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)
Watch BP pulse BUNcreatinine and urinary output
Use plasma expandersblood if in shock and does not respond quickly to saline
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia dehydration and acidosis-producing derangements in intermediary metabolism including production of serum acetone
Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin
deficiencydependence The presenting symptom for ~ 25
of Type I Diabetics
Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin
Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation
Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations
respiratory distress Abdominal tenderness (may resemble
acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema
possibly coma
INSULIN Administer short-acting insulin IV (01
unitskg) or IM (03 unitskg) then 01 unitskg per hour by
continuous IV infusion Increase 2- to3-fold if no response by 2ndash
4 h If initial serum potassium is lt 33
meqlcorrect K level while giving insulin to prevent dangerous hypokalemia
Expected fall is 50-100 mgh Transition into SQ when
A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO
FLUID1 Deficit is around 6-8 L ndash need NOT to
replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over
first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash
300mLh Change to 5 glucose and 045 saline
at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)
Watch BP pulse BUNcreatinine and urinary output
Use plasma expandersblood if in shock and does not respond quickly to saline
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin
Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation
Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations
respiratory distress Abdominal tenderness (may resemble
acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema
possibly coma
INSULIN Administer short-acting insulin IV (01
unitskg) or IM (03 unitskg) then 01 unitskg per hour by
continuous IV infusion Increase 2- to3-fold if no response by 2ndash
4 h If initial serum potassium is lt 33
meqlcorrect K level while giving insulin to prevent dangerous hypokalemia
Expected fall is 50-100 mgh Transition into SQ when
A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO
FLUID1 Deficit is around 6-8 L ndash need NOT to
replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over
first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash
300mLh Change to 5 glucose and 045 saline
at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)
Watch BP pulse BUNcreatinine and urinary output
Use plasma expandersblood if in shock and does not respond quickly to saline
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation
Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations
respiratory distress Abdominal tenderness (may resemble
acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema
possibly coma
INSULIN Administer short-acting insulin IV (01
unitskg) or IM (03 unitskg) then 01 unitskg per hour by
continuous IV infusion Increase 2- to3-fold if no response by 2ndash
4 h If initial serum potassium is lt 33
meqlcorrect K level while giving insulin to prevent dangerous hypokalemia
Expected fall is 50-100 mgh Transition into SQ when
A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO
FLUID1 Deficit is around 6-8 L ndash need NOT to
replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over
first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash
300mLh Change to 5 glucose and 045 saline
at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)
Watch BP pulse BUNcreatinine and urinary output
Use plasma expandersblood if in shock and does not respond quickly to saline
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations
respiratory distress Abdominal tenderness (may resemble
acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema
possibly coma
INSULIN Administer short-acting insulin IV (01
unitskg) or IM (03 unitskg) then 01 unitskg per hour by
continuous IV infusion Increase 2- to3-fold if no response by 2ndash
4 h If initial serum potassium is lt 33
meqlcorrect K level while giving insulin to prevent dangerous hypokalemia
Expected fall is 50-100 mgh Transition into SQ when
A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO
FLUID1 Deficit is around 6-8 L ndash need NOT to
replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over
first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash
300mLh Change to 5 glucose and 045 saline
at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)
Watch BP pulse BUNcreatinine and urinary output
Use plasma expandersblood if in shock and does not respond quickly to saline
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
INSULIN Administer short-acting insulin IV (01
unitskg) or IM (03 unitskg) then 01 unitskg per hour by
continuous IV infusion Increase 2- to3-fold if no response by 2ndash
4 h If initial serum potassium is lt 33
meqlcorrect K level while giving insulin to prevent dangerous hypokalemia
Expected fall is 50-100 mgh Transition into SQ when
A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO
FLUID1 Deficit is around 6-8 L ndash need NOT to
replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over
first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash
300mLh Change to 5 glucose and 045 saline
at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)
Watch BP pulse BUNcreatinine and urinary output
Use plasma expandersblood if in shock and does not respond quickly to saline
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
FLUID1 Deficit is around 6-8 L ndash need NOT to
replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over
first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash
300mLh Change to 5 glucose and 045 saline
at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)
Watch BP pulse BUNcreatinine and urinary output
Use plasma expandersblood if in shock and does not respond quickly to saline
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
ELECTROLYTES1 The critical is K2 There is always a deficit but blood
levels may be low normal or high 3 Frequent EKG and serum levels are
mandatory 4 Initially IV may be the only way to
administer K but remember that once PO is re-established K can be given orally
Factors reducing serum K+ 1048698 Rehydration rarr uarr urinary secretion of
K+ 1048698 Insulin administration moves K+ from
extracellular to intracellular
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Replace K+ 10 meqh when
plasma K+ lt 55 meqL ECG normal urine flow and normal Cr
40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given
SERUM K Rate hour LOW (lt35) 40 Meq
Normal (35-50) 20 Meq Normal pH lt70 or
EKG changes 40 Meq
High (gt50) Hold until level normal
High (gt50) pH lt 70 or EKG changes
10-20 meq
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
BICARBONATE1 Usually NOT necessary2 It may even be dangerous and
precipitate hypokalemia cerebral acidosis and cardiac dysfunction
3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction
If needed 20-30 mEql potassium phosphate can be given
Broad spectrum antibiotic coverage is required
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)
amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid
intake and output every 1ndash4 h Assess patient What precipitated the episode (noncompliance
infection trauma infarction cocaine) Initiate appropriate workup for precipitating event
(cultures CXR ECG) Continue above until patient is stable glucose goal
is 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01
unitskghr
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation
with hyperventilation Shock
If not improving with fluids ro MI
Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days
after DKA
Pulmonary Edema and Hypoxemia
Iatrogenic hypoglycemia and hypokalemia
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent
Adequate amount of crossmatched blood is kept ready
The standard monitors attached HGTCVP and urine output monitoring is essential
IV fluid is attached
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc
Excellent analgesiano need to use NSAIDS or opiods intra op
Hypoglycemia amp hyperglycemic coma can be detected early
Avoidance of ETT amp resultant infection
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Disadvantages Inadvertant higher level of block can
result in hypotension complicated by autonomic neuropathy in DM
Sympathetic blockade can impair control of insulin secretion
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Femorosciatic nerve block can be given which helps prevent hypotension and also provides superior intra and post op analgesia
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Epidural anaesthesia either single shot or catheter in situ can be used to avoid hypotension and also for post op pain relief
Disadvantage includes risks of infection and vascular damage
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
For small ulcers confined to foot ankle block using Inj Bupivacaine and Inj Lignocaine can be given
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Aspiration prophylaxis is given with antacid and antiemetic
Rapid sequence induction should be done in case of inadequate starvation or autonomic neuropathy(gastroparesis)
Muscle relaxant Rocuronium should be used instead of Sch ico hyperkalemia
After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes
Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane
Reversalroutine reversal Extubation after adequate recovery of
airway reflexes Post op monitoring blood sugar
levelserum and urine ketones serum electrolytes