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286 Cards in this Set
- Front
- Back
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the upper GI tract anatomy includes
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pharynx
upper esophageal sphincter body of the esophagus diaphragm lower esophageal sphincter stomach duodenum |
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Sucralfate (Carafate®) and GERD
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Acts a a protective agent
Main component is: ___Al______________ Role is limited, but may be used as adjunctive therapy for severe esophagitis Requires 4 times a day dosing (1 g per dose) Constipation and chelation of other drugs Avoid in renal disease |
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Define stress related mucosal disease
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Stress related mucosal disease (SRMD)
Erosive process if the gastroduodenum that occurs with abnormally high physiologic demand |
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what is the difference between erosion and ulcer with SRMD
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erosion is in the mucosa layer, where as an ulcer is into the submucosa and when if hits cappilaries or vessels you get a bleed
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Major stressful events include
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surgery, trauma or sepsis
Not anxiety/exam related stress Different from GERD or PUD Lesions are multiple and develop in the gastric fundus |
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Lesions may be ___________ or __________
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asymptomatic or symptomatic
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with SRMD where do lesions typically develop
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in the gastric fundus, but can develop in the duodenum, which are more erosive and are associtaed with larger bleeds
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Overt bleeding definition
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Hematemesis, bloody gastric hematemesis, aspirate (when pulling out an NG tube), hematochezia, coffee ground emesis, guaiac positive stools
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Clinically important bleeding (overt +) defintion
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SBP drop > 20 mm Hg
SBP drop > 10 mm Hg + ↑ HR 20 bpm ↓ Hemoglobin > 2 gm/dL (or will not correct with a transfusion) Failure of hemoglobin to correct with transfusion Gastric bleeding requiring surgery |
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How does SRMD differ from PUD or GERD
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SRMD usually has multiple lesions where GERD and PUD ususlly only have one primary lesion
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Symptoms of overt and clinically important bleeding
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Overt: erosion of mucosa to vessel <25%
Clinically important, deeper erosion, exposing a larger vessel <6% ranges from 0.1-39%, inc morbidity, mortality > 50% increased icu day by 11 days!!! |
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Incidence SRMD
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Erosions within first 24 hrs of ICU admission (starts early on)
Clinically important bleeding: 0.1- 39% (6%) (small chance, but more thatn 50% of the time it is fatal) Trials from 2000 to current range 0.1-4% Clinically important bleeding vs. overt bleeding Critically ill patients mortality rate – 48.5% w/ vs. 9.1% w/o bleed |
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what cells produce H+
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parietal
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what cells produce pepsinogen
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chief
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what activates pepsinogen
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an acidic enviroment
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what do PG produce to prevent insult to the stomach lumen
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bicarb and mucus gel layer
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what does blood flow provide the GI tract with
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O2 and nutrients and removes waste materail
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Pathophysiology of GI tract
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Reduced microcirculatory blood flow
altered normal protective mechanisms - decrease in nutrient and O2 delivery--> decrease proliferation and cellular turnover of gastric mucosa--> decrease bicarb efflux and mucus secretion into the gastric epithlium with a decrease in PG As a result: inability of the mucosa to remove and neutralize gastric acid |
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diagnosis of SRMD
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Overt or clinically important bleeding
Nasogastric tube suctioned contents Confirmed with EGD (esophagogastroduodenoscopy) |
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the 2 major risk fators for SRMD
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respitatory failure (mechanical ventilation and Coagulopathy
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Risk Factors for SRMD
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Major risk factors
Mechanical ventilation > 48 hours Coagulopathy (INR > 1.5; Platelets < 50,000; aPTT > 2x control) Minor risk factors Hypotension Sepsis Other risk fators: GI ulcer or bleeding within past year Renal failure Hepatic failure Head injury Trauma/ major surgery Burns ≥ 35% of TBSA Recent solid organ transplant High dose corticosteroids (250mg/day hydrocortisone or equivalent) |
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goals of prophylaxis treatment for SRMD
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Reduce morbidity and mortality by preventing clinically significant bleeds
Choose an agent that provides optimal efficacy with minimal adverse effects Focus on “ICU” side-effects Choose an agent that is the most cost effective. the agent should be fast acting and easy to give and have the fewest possible SE |
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Pharmacologic Agents for SRMD
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Antacids
Historical purposes only Sucralfate Histamine H2-Antagonists (H2RA) Proton Pump Inhibitors (PPI) Enteral nutrition |
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mechanical ventialtion causes SRMD by
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high PEEP (positive end expiratory pressure) that decreases CO so there is a decrease in splanchnic profusion
there is a release of pro-inflammatory cytokines released that alters GI motility There is a systemic activationof increased ACh to cause splanchnic hypoprofusion splanchnic hypoprofusion causes altered GI motility and mucosal injury all leading to SRMD |
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sucralfate and antacids acit by
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Sucralfate
(physical barrier) Antacids (neutralizes acid) |
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PPIs inhibit
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the atpas proton pump
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Antacids
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MOA:
Neutralizes intragastric acid Stimulates prostaglandin synthesis Dosing: Al(OH)3/Mg(OH)2 (Maalox®): 30-60 mL po Q1-2 H to achieve pH control Advantages: Rapid, easily titrated, controls pH, cost Disadvantages: Frequent dosing, no IV form, aspiration risk |
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SE of antacids
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Diarrhea, constipation, hypophosphatemia,
hypermagnesemia (renal insufficient), hypercalcemia, metabolic alkalosis, aspiration |
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interactions with antacids
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(decreased absorption)
Fluoroquinolones, tetracyclines, iron, H2 antagonists |
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Sucralfate
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Polymerizes and selectively binds to necrotic
ulcer tissue (requires acidic pH for activation) Binds to gastric acid, pepsin and bile acids Dosing 1 gram po Q6H Advantages No pH monitoring, enhances defense factors, lower theoretical risk for nosocomial pneumonia and cost Disadvantages No IV formulation, drug interactions, frequent dosing |
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SE of sucralfate
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Aluminum retention may occur in renal
insufficiency |
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interations with sucralfate
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Decreased absorption of many drugs:
Fluoroquinolones, tetracyclines, theophylline, phenytoin, antacids, digoxin, amitriptyline ►Separate administration out by 2 hours |
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H2RAs
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Competitive reversible inhibitor of H2-receptors on parietal cells thus decreasing gastric acid secretion
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how are H2RAs dosed for SRMD continuous or bolus
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bolus because there is less of a risk for pneumonia and it still prevents the risk of a bleed
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H2RAs advantages and disadvantages for SRMD
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ADVANTAGES
Oral/IV formulations, ease of dosing, clinical data, costs DISADVANTAGES Side effects, nosocomial pneumonia potential Cimetidine approved but avoided due to CYP-450 drug interactions, Interaction w/ medications requiring acid to be absorbed |
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SE of H2RAs
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HA, confusion, dizziness, hallucinations, diarrhea, thrombocytopenia (not very common: would take about 5 days to occur because have to produce that haptens that the body generates an allergic reaction against), agranulocytosis, rash, infusion-related hypotension
“Pneumonia potential” |
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PPIs: MOA, advantages and diadvantages for SRMD
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MOA
Irreversible inhibitor of gastric parietal cell H/K ATP pump More potent acid inhibition than H2 antagonist ADVANTAGES Oral/IV formulations, ease of dosing, clinical data, pH control, +/- drug interactions DISADVANTAGES Cost, nosocomial pneumonia potential, C. difficile association |
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SE of PPIs
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Headache, possible risk of pneumonia, possible association with C. difficile
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drug interactions with PPIs
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Drug Interactions
Decreased absorption medications requiring acidic pH for absorption |
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do we monitor pH for SRMD
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no
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Stress Ulcer Prophylaxis Monitoring
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PPI more effective in maintaining gastric pH > 4 during its dosing interval vs. H2-antagonist
Occasional acidic environment might not be bad Pleotrophic effects of H2-antagonist Monitor for signs of bleeding SBP HR HgB /Hct Monitor for signs of toxicity and drug interactions |
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comparitive studies have shown for SRMD
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Numerous studies have demonstrated
positive effect of pharmacological agents for stress ulcer prevention Few studies have definitely establish thesuperiority of one agent versus another |
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Meta-Analysis
Overt Bleeding results for SRMD |
significant results with:
H2RA vs. placebo H2Ra vs. antacid sucralfate vs. placebo but no significant results with sucralfate vs. H2RA |
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Meta-Analysis
Clinically Important Bleeding results for SRMD |
Antacids with stronger effect compared with overt bleeding (0.66) but has wider CI here
H2RAs trending to superiority against placebo or antacids Sucralfate showing no distinguishable superiority compared to H2RAs or antacids, but sample size too small for precision No statistically heterogeneity |
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Meta-Analysis
Nosocomial Pneumonia results for SRMD |
Sucralfate trend towards lower incidence of PNA compared to antacids or H2RAs
H2RAs associated with higher incidence of PNA when compared to no prophylaxis; no difference compared to antacids Sucralfate trend towards increase PNA compared with no prophylaxis? there is not difference in the agents that cause pneumonia |
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Meta-Analysis
Mortality results for SRMD |
Compared to antacids or H2RAs, sucralfate has a trend toward a decrease in mortality
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Sucralfate vs. Ranitidine In Patients Requiring Mechanical Ventilation for SRMD
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Largest randomized trial for stress ulcer patients
1200 patients requiring > 48 hours of mechanical ventilation Randomized to treatment consisting of: Ranitidine 50 mg IV Q 8H (renal dose adjusted) Sucralfate 1000 mg NG Q6H less bleeds with ranitidine were significant no difference in pneumonia |
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Omeprazole vs. Cimetidine for SRMD
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Randomized, double-blind, double-dummy, non-inferiority trial (the study wasn't powered to show the benefits of one agent over the other)
Oral omeprazole 40mg daily vs. IV cimetidine 300mg bolus then 50mg/hr (titrated to pH) Mechanically ventilated 10 endpoint: “Clinically significant bleed” BRB from tube after 5-10 min lavage (saline lavage is like a saline rinse) 8 hr Gastroccult+ coffee-ground aspirate 2-4 hrs Gastroccult+ aspirate days 3-14 Planned analysis of median gastric pH and nosocomial pneumonia Conclusion: PPIs are useful for stress ulcer prophylaxis, but H2RA’s remain the drug of choice |
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Nosocomial Pneumonia Risk and Stress Ulcer Prophylaxis
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Comparison of Pantoprazole vs Ranitidine in Cardiothoracic Surgery Patients
Retrospective cohort analysis Primary Outcome: Incidence if nosocomial pneumonia Pantoprazole group: n = 377 Ranitidine group: n = 457 Results: Incidence of UGB similar in both groups 0.8% in pantoprazole group vs. 0.2% in ranitidine group (p = 0.333) Incidence of nosocomial pneumonia Propensity analysis: pantoprazole treatment was found to be an independent risk factor for nosocomial pneumonia (p = 0.034) the sicker patients were put on a PPI so they had a greater risk of developing pneumoia overall |
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AB has an oral-gastric tube placed and ready for use. What is the most appropriate recommendation to make regarding stress ulcer prophylaxis for AB?
Sucralfate 1GM FT Q6h Maalox 30ml FT Q2h Esomeprazole 40mg FT Daily Famotidine 20mg FT BID |
Famotidine 20mg FT BID
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Conclusions about SRMD
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Stress ulcers are associated with significant morbidity/mortality
Only patients with risk factors for stress ulcers should receive prophylaxis H2RA’s are considered the drug of choice PPI’s are likely efficacious but may not be superior to H2RA’s and may carry risks |
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nausea defintion
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“unpleasant sensation of the imminent need to vomit….; a sensation that may or may not lead to the act of vomiting”
Subjective in nature patient does not typically vomit perception |
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vomitting defintion
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“Forceful expulsion of gastric contents associated with contraction of the abdominal and chest wall musculature”
does not have to be accompanied with nausea not a common SE with most drugs chemo drugs and antibiotics are the drugs most likely to cause |
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regurgittaion definition
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the act by which food is brought back into the mouth without the abdominal and diaphragmatic muscular activity that characterizes vomiting”
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retching defintion
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“Spasmodic respiratory movements against a closed glottis with contractions of the abdominal musculature without expulsion of gastric contents”
AKA: “dry heaves” |
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eitiology of N/V
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visceral stimuli--> Dopamine and 5HT released--> medullary vomitting center stimulated--> N/V
chemoreceptor trigger zone--> Dopamine and 5HT released--> medullary vomitting center stimulated--> N/V vestibular input--> histamine and Ach released-->medullary vomitting center stimulated--> N/V |
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what are the major recepotrs involved in N/V
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D2, 5HT, H2
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Nausea and Vomiting Greatest Hits
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Infectious
Viral or bacterial gastroenteritis, otitis media, meningitis GI Pancreatitis, gastroparesis, cholecystitis Hepatitis, appendicitis, cancer PUD, gastric outlet obstruction IBD, IBS CNS Migraine, stroke, seizures, cancer Pain Motion sickness Endocrine/metabolic Pregnancy Uremia Thyroid disease Diabetes Cardiovascular Myocardial infarction Heart failure Alcohol and illicit drug use and withdrawal Post-operative (PONV) |
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Common Drug Causes of N/V
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Chemotherapeutic agents
Opiates (particularly IV) All can cause N/V Morphine (most likely to cause N/V out of this class), oxycodone, meperidine, fentanyl NSAIDs Colchicine Digoxin Often one of the first signs of toxicity Estrogens, progesterone Oral contraceptives, megesterol (not as big as a problem now because birth controls have lower doses) Antibiotics Macrolides (erythromycin, clarithromycin) Sulfonamides (trimethoprim/sulfamethoxazole) Metronidazole Sulfasalazine Dopamine agonists Levodopa Pramipexole, ropinirole, bromocriptine |
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Clinical Consequences of N/V
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Dehydration
Aspiration Electrolyte and acid base disturbances Mallory-Weiss Syndrome--> a tear in the musculature of the esophagus at the junction of the stomach, which can cause bleeding. Thet usually heal on their own Loss of productivity Extension of hospital admissions |
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Appropriate Referrals for N/V
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Severe dehydration
Protracted vomiting (> 1-2 days) Infants or frail elderly Severe headache +/- stiff neck +/- fever Recent head injury Evidence of blood in vomitus Severe abdominal pain or distension Behavioral or mental status changes Ingestions |
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signs of dehydration
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sucken eyes
poor skin tuger (but it is possible they may jus thave dry skin) altered mental status dizziness low BP constipation decreased urine output |
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General Management of N/V
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Treating the underlying disorder(s) may reduce N/V
Oral rehydration appropriate for all patients if tolerated may be difficult in severe cases = need for IV * gateraid dilute 50/50 May combine drugs with different MOA Patients may need alternative dosage forms if vomiting frequently IV, SC SL, transdermal Rectal |
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OTC N/V drugs are good for what type of N/V
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mild
motion sickness |
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Prochlorperazine (Compazine®)*
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Phenothiazine (dopamine antagonist D2 receptor)
Tablets (5 mg, 10 mg): dosed 3-4 times/day Sustained release capsules 10 mg every 12 h or 15 mg once daily Suppositories (2.5 mg, 5mg, 25mg) Syrup (5mg/5ml) IV/IM (DO NOT inject subcutaneously) Can be used for age > 2 years or > 20 lbs Pregnancy category C EPS, sedation, hypotension (IV), tissue irritation works quickly for more severe vomitting |
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EPS
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extra parametal sympotoms
parkason like sympotoms--> tremor |
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Promethazine (Phenergan®)*
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Phenothiazine: antidopaminergic, antihistamine, anticholinergic properties
Tablets (12.5 mg, 25 mg, 50 mg) Suppositories (12.5 mg, 25 mg, 50 mg) Injection (DO NOT inject subcutaneously) Dose = 12.5-25mg every 4-6 hours 1/10th the dopaminergic blockade vs. chlorpromazine Can be used for age > 2 years Pregnancy category C EPS, sedation, hypotension (IV), tissue necrosis (must be diluted), anticholinergic effects sedation is more common than with prochlorperazine because this is an antihistamine |
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Choosing a Phenothiazine
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why choose prochlorperazine:
different dosage forms ok for kids and pregnancy (short term) less sedating quick onset with in 30 minutes for severe vomitting chemo patients only one with a SR formulation why choose promethazine: different dosage forms ok for kids and pregnancy (short term) quick onset with in 30 minutes for mild N/V good for nausea associated with inner ear dysfunction |
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Metoclopramide and N/V
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May be used when delayed gastric emptying
IV and Oral IR tablets Metolzolv ODT® 5 mg and 10 mg tablets No liquid required FDA approved for diabetic gastroparesis and GERD (increases esophageal CL0 CNS effects, limit dose and duration good for DM when there is nerve damage because it results in delayed gastric emptying adjunct only in severe cases |
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Ondansetron (Zofran®)
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seratonin antagonist
IV formulation Oral tablets (4mg, 8mg) Oral disintegrating tablet (ODT): no liquids required shorter acting Oral Solution (4mg/5ml) |
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Granisetron (Kytril®):
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serotonin antagonist
IV solution Oral tablet (1 mg) Oral solution (2 mg/10 ml) shorter acting |
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Dolasetron (Anzemet®)
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serotonin antagonist
IV solution Oral tablets (50 mg, 100 mg) |
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Palonosetron (Aloxi®)
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IV solution
Much longer acting (up to 24 hours - 5 days) One dose vs. other agents good for chemo patients prevention of delayed onset N/V |
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Serotonin antagonist major clinical uses for N/V
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Chemotherapy induced
Radiation induced Prevention of post-operative Hospitalized patients Well tolerated: QTc prolongation at high doses $$$$$ |
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antihistamines and N/V
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Dimenhydrinate (Dramamine®)
Cyclizine (Marezine®, Bonine for Kids®) Take 30-60 minutes prior, may dose every 4-6 hours Meclizine (Bonine®, Antivert®, Dramamine Less Drowsy®) 25-50 mg 60 minutes prior, may dose every 24 hours Dosed more frequently for vertigo Doxylamine (Unisom®) 25 mg tablets, 50mg capsules Sedation and anticholinergic adverse effects Avoid with ETOH, CNS depressants, and in kids take 30 minutes to an hour prior to exposrantihistamine effects help the inner ear good for motion sickness prevents doesn't treat |
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anticholinergics
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Scopolamine (Transderm-Scop®)
Indicated for motion sickness and PONV can cause halucinations not as sedating as antihistmines |
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Appropriate use
for a scopolamine patch |
Apply behind ear 4 hours prior to travel
Apply evening prior to surgery Apply 1 hour prior to C-section Wash hands after applying May wear for 72 hours Change ears if using > 72 hours Don’t cut patch |
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Phosphorylated Carbohydrate Solution (Emetrol®)*
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Phosphoric acid (21.5mg), dextrose (1.87g), fructose (1.87g)
Avoid in diabetes and fructose intolerance MOA: Hyperosmolar solution May have direct effects that ↓ smooth muscle contraction and delay gastric emptying time Dose 5-10 ml (kids) or 15-30 ml (adults) every 15 minutes Use undiluted for best effect Don’t use > 1 hour (or max of 5 doses) the affects are related to the osmolarity so do not dilute it is not systemically absorbed |
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Non-Drug Measures fo N/V
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Acupressure wristbands
Seaband® ReliefBand® Stimulation of the pericardium 6 (P6) point Effective within 5 minutes Can use for all types of nausea Can use with antiemetic drugs May use SeaBand® in kids > 3 years old effects are variable not good recomendation for the flu adjuct not first line therapy |
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Gastroenteritis Induced N/V
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The flu
Self limited in most cases May also need an antidiarrheal drug Oral rehydration Drug options Phosphorylated Carbohydrate Solution Dopamine antagonists Chlorpromazine or promethazine Serotonin antagonists in severe cases (otherwise to potent for the flu) |
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N/V of Pregnancy (NVP) options
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Pyridoxine (Vitamin B6)
10-25 mg 3-4 times a day (usually administered with the antihistamine) Phosphorylated Carbohydrate Solution (not good for chronic) Antihistamines Promethazine Doxylamine 12.5mg 3-4 times/day (200mg/day max) Dimenhydrinate Phenothiazines or metoclopramide Acupressure |
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N/V of Pregnancy (NVP)
Try non-pharmacologic measure first |
Fresh air in bedroom
Eating crackers prior to getting out of bed slowly Smaller, more frequent meals Avoid high fat meals and spicy foods Chilled vs. hot food may be less nauseating |
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N/V of Pregnancy (NVP)
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70-85% of pregnant women
Hyperemesis Gravidarum (0.5%) May be due to increases in B-HCG |
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Motion Sickness
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Vestibular mediated
Non-pharmacologic measures Avoid reading during travel Keep line of vision straight ahead Avoid excessive food and alcohol prior to travel Sit: front of car, mid-ship, or over wing of plane |
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drugs of choice for motion sicknes
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Drugs of choice
Scopolamine Antihistamines |
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Post-Operative N/V (PONV)
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Affects ~30% of patients within 24 hours of surgery
Major contributing factors Intestinal irritation and stasis Use of general anesthetics (stimulate CTZ) Use of volatile anesthetics (e.g. nitrous oxide) Use of post-op narcotics |
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Post-Operative N/V (PONV) risk factors
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Risk factors
Female sex, history of PONV, non-smoker Abdominal, gynecologic, and ENT procedures Longer duration of surgery |
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Prevention of PONV
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Focus on prevention; target higher risk patients
Drugs of choice = serotonin antagonists Ondansetron 4 mg IV immediately prior to anesthesia 16mg orally one hour prior to anesthesia Granisetron 1mg IV immediately prior to anesthesia Dolasetron 12.5mg IV 15 min prior to cessation of anesthesia Palonosetron 0.075 mg IV immediately prior to anesthesia Also work best to treat N/V after surgery Alternatives Scopolamine, promethazine, acupressure |
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what is the drug of choice given prior to surgery to prevent PONV
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serotonin antagonist
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PN considerations
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Previous PN concepts
Assessment, estimating needs, calculations, protein, refeeding Focus on other macronutrients and micronutrients Sources of energy CHO (dextrose): D50 or D70 = Dextrose 50% or 70% AA (protein/N+): CAA (crystalline amino acids) = 10% or 15% solution IVFE (intravenous fat emulsion)= Fats 10 - 20% Access sites: peripheral and central Standard order forms, QA, monitoring |
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Parenteral Nutrition (PN)Common names
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Hyperalimentation (hyperal)
TPN (total parenteral nutrition) TNA (total nutrient admixture) PPN (peripheral parenteral nutrition) CPN (central parenteral nutrition) 2:1 vs 3:1 compounded solutions |
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lipid contribution to the npc
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Used to QS energy estimates once protein needs met
Provide at least 2 – 4% of calories from lipid to prevent essential FA deficiency Do not exceed 30% of calories from lipid at risk of hypertriglyceridemia Limit to 1 gm/kg/day |
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CHO contribution to the npc
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Use to QS energy estimates once protein/lipid needs met
Using >20 - 25 kcal/kg/day exceeds oxidation rate (metabolic complications from too much sugar) Infusion rates > 5 mg/kg/min increase complications from excess |
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NPC
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non-protein calories
CHO and fat |
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Lipid emulsion
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10% solution contains 1.1 kcal/ml
20% solution contains 2 kcal/ml (most common) Preferred for TPN formulation Volume used X 2 = calories provided from fat Most institutions have standard volume on PN order Non-IV fats = 9 kcal/gm (IV is 2 kcal/ml) a.k.a lipids, fats, fatty acids, IVFE, fat emulsion, intralipid TG source soybean/safflower oil, egg phospholipids (emulsifier) and glycerol (adjusts tonicity) contributes calories to account for differences in IV White solution Usually 200-250 cc of lipids in PNTG source soybean/safflower oil, egg phospholipids (emulsifier) and glycerol (adjusts tonicity) contributes calories to account for differences in IV White solution Usually 200-250 cc of lipids in PN |
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excessive Lipids
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Hypertriglyceridemia
Pancreatitis Immunosuppression Altered pulmonary hemodynamics (excess CO2 production and altered breathing rates) |
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monitoring and adjusting lipids
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Serum TG at least weekly
Consider temporary interruption if TG > 275 mg/dL (back off so liver can clear out the excess lipids) Give lipids QOD or infuse separately over 12 hours If serum TG > 400, withhold lipids and monitor (check liver enzymes and do a lipid panel) |
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lipid deficiency
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Lipid deficiency (EFAD)
Alterations in PLT function, GI mucosa dysfunction Hair loss Poor wound healing Dry, scaly skin, desquamative dermatitis EFAD (linoleic acid and α-linoleic acid) can be prevented by providing 2 - 4% of calories from fat, or approximately 100 g/week. Obese patients still need calories from fat! |
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Propofol
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Propofol is an IV sedative/anesthetic agent (stabilized by lipid emulsion)
“milk of amnesia” Essentially 10% lipid emulsion Contributes 1.1 kcal/ml infused Can add significantly to daily calorie/fat intake |
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Patient receiving propofol at 15 ml/hr
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15 ml/hr x 24 hrs/day = 360 ml/day
360 ml/day X 1.1 kcal/ml = 396 kcal lipid/day (so a reason to withhold lipids or cut in ½) Almost the same as adding 200 ml 20% lipid to TPN |
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Dextrose for PN
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Stock solutions of dextrose monohydrate 50% or 70% for compounding
% = gm/100 ml 1 gm hydrated dextrose = 3.4 kcal (orally = 4 kcal/gm) If PN interrupted, a stock bag of D10% (bridge bag) should be hung at the same rate to prevent rebound hypoglycemia when CHO infusion suddenly stops for >1 hr (then taper the infusion slowly to prevent the rebound hypoiglycemia) |
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1 gm hydrated dextrose =
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3.4 kcal iv (orally = 4 kcal/gm)
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CHOs
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Use to QS remaining calories (primary energy)
Most institutions have standard orders Excess carbohydrates: Hyperglycemia, endocrine abnormalities Insulin resistance (over time) Lipogenesis, excess CO2 production Fatty liver infiltration (increases in LFTs) Monitor blood glucose q4-6 hours (if an increase in rate or a change in [] check) Consistent elevations may warrant insulin or cutting down on CHOs Represents the bulk of the calories |
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Fluid requirements
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Can meet daily needs via PN if desired
Evaluate needs: Edema Ascites Skin turgor Mucous membranes Ins versus Outs (I/O) urine output Insensible/abnormal losses: respiration, wounds (evaporation), fever (evaporation), emesis, NG suction, diarrhea, etc. Monitor: UOP, weight, electrolytes, CV function, IV’s |
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Fluid estimates
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25 -35 ml/kg/day maintenance
~1 ml fluid / kcal ingested To meet needs with PN, sterile H2O is added to create the extra volume If cost is issue (PN charged based on volume) Don’t account for extra volume in PN Use commercially available IVF solution and infuse separately (D51/2NS, NS, D5NS, e.g. most are 5% solutions so not many calories, but watch for patients on multiple drips they add up over the course of time so can switch to NS to avoid extra dextrose) |
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Volume to infuse
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Can determine initially based on fluid needs:
Recall 1 ml/kcal or ~ 25-35 ml/kg/day Estimate 2000 ml/day = PN infused at 83 ml/hr Estimate 2000 kcal/day ~ 2000 ml PN solution PN can provide only the volume needed to contain the macro/micronutrients, divided over 24 hours Additional fluid needs met with stock IVF solutions infused separately 1500 ml PN, estimated fluid needs are 2500 ml Need @ 1000 ml extra to meet needs Infuse D5NS at 50 ml/hr = additional 1200 ml/day Account for extra fluid sources: IV fluids, drips and vehicles |
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PN micronutrients
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Electrolytes
Maintain normal serum concentrations Standard/customizable on formula order forms Monitor lab trends, adjust according to condition Vitamins/Trace minerals Routinely added to approximate the daily intake requirements for a healthy adult Consider clinical condition to adjust components Be aware of compatibility and stability issues |
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Vitamins (MVI) for TPN
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Standard water and fat-soluble vitamins added daily (10ml)
Most preparations contain 12-13 vitamins per RDA MVI-12 does not contain Vitamin K Potential drug-nutrient reaction Act as catalysts and substrates for metabolic reactions Generalized malnutrition can cause multiple deficiencies/altered requirements Individual deficiencies: Thiamine- Wernicke’s encephalopathy(CNS demylenation) (ETOH/alcoholics) B12 (cyanocobalamin)- pernicious anemia lack of absorption Folic acid: megaloblastic anemia (hemotologic abnormalities) Pregnancy and deficiency in folic acid want to prevent neural tub defects Fat soluble ADEK: Stored by body, risk of hypervitaminosis (vitamin A can be problamatic) |
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fat soluble vitamins
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ADEK
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individual deficiencies in vitamins
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Thiamine- Wernicke’s encephalopathy(CNS demylenation) (ETOH/alcoholics)
B12 (cyanocobalamin)- pernicious anemia lack of absorption Folic acid: megaloblastic anemia (hemotologic abnormalities) Pregnancy and deficiency in folic acid want to prevent neural tub defects |
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Trace elements:
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Provide daily requirements for essential trace minerals
Zinc, copper, chromium, manganese ± selenium, molybdenum or iodide Iron not included (compatibility/stability concerns) trivalent will disrupt the lipids Important function as co-factors for metabolic pathways Multiple deficiencies/altered needs can present Manganese and copper secreted through biliary tract so not good in hepatic impairment over time Selenium and chromium are excreted renally not good for renally impaired Zinc, copper and selenium: GI malabsorption and cutaneous losses (burns) Long-term PN: concern for trace element toxicity Typical addition of 1 ml trace element concentrate/bag PN Administration can administer on a weekly basis rather than every day |
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Electrolytes:
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Na+, K+, Ca++, Mg++, Phos, Acetate, Cl- (acetate and Cl are the anions)
Give for maintenance or to correct deficits Amount varies with age, organ function, nutrition status, drug therapy, condition Standard amounts/reference ranges on order forms Cl- and acetate used for acid-base balance Acetate has the same alkalinizing power of bicarbonate (add more in the patient is acidodic, if the patient is alkalotic add more Cl) Utilize chloride and acetate “salts” of other lytes NaCl/NaAce/NaPhos; KCl/KPhos/KAce; CaGluc; MgSO4 |
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Cl- and acetate used for acid-base balance
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Acetate has the same alkalinizing power of bicarbonate (add more in the patient is acidodic, if the patient is alkalotic add more Cl)
Utilize chloride and acetate “salts” of other lytes NaCl/NaAce/NaPhos; KCl/KPhos/KAce; CaGluc; MgSO4 |
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what are the anions added to TPN
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Cl and acetate
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Electrolyte disturbances
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Losses through the GI tract (emesis, diarrhea)
Na+, Cl-, K+, HCO3 Dependent on renal function Na+, K+, Mg++, Phos retention; Ca++ depletion Drug-nutrient interaction Diuretics/loops- urine Na+, K+, Mg++ wasting Potassium-sparing diuretics/ACE/ARB- K+ retention |
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what electrolytes should you watch for with refeeding syndrome
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K+, Mg++, Phos total body depletion
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standared requirements for electrolytes
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Na 1-2mEq/kg
K 1-2 mEq/kg Ca 5-15 mEq (~5-10 mEq/L) Mg 8-24 mEq (~5-10 mEq/L) Phos 20-45 mmol (~2-20 mmol/L) Cl-/acetate balance for acid base 1:1 |
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Standard order states: Sodium 30 mEq/L
Total volume of bag = 2.4 L |
Total sodium: 2.4 L x 30 mEq/L = 72 mEq Na+
Stock solution of NaCl = 4 mEq/ml 72 mEq x 1 ml/4 mEq = 18 ml |
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Standard order states: 5 mmol Phos/L
Total volume of bag = 2.4 L Use potassium phosphate = 3 mmol/ml Phos |
Total phos = 2.4 L x 5 mmol/L = 12 mmol Phos
Use potassium phosphate = 3 mmol/ml Phos 12 mmol X 1 ml/3 mmol = 4 ml What about the potassium? 4.4 mEq/ml KPhos solution 4 ml x 4.4 mEq = 17.6 mEq K+ (have to take patients K levels into account) |
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Dextrose: 200 g/L ordered, TRA 80 ml/hr, use 70%
70 kg patient |
80 ml/hr x 24 hrs = 1920 ml/day = 1.92 L
200 g/L x 1.92 L = 384 g dextrose 384 g x 100 ml/70 g (70%) = 548 ml Double check: 548 ml X 70 gm/100 ml = 383.6 gm√ Calories: 384 g x 3.4 kcal/g CHO = 1305.6 kcal from CHO (3.4 because IV) |
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what rate of administration do you not want to exceed for dextrose
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Excess rate of administration = 5 mg/kg/min
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Compound calculations % example
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Admixture can be ordered in percentage:
Dextrose final concentration = 20% Determine amount of CHO (g) provided for that PN solution infusing at 80 ml/hr over 24 hours 80 ml/hr x 24 hrs = 1920 ml = 1.92 L 20% = 20 g/100 ml 1.92 L = 1920 ml X 20 g/100 ml = 384 g CHO 384 g CHO x 3.4 kcal/gm = 1305.6 kcal |
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Compound calculations for protein
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Protein: 50 g/L, TRA 80 ml/hr, 10% solution
80 ml/hr x 24 hrs = 1920 ml = 1.92 L 50 g/L x 1.92 L = 96 g protein 96 g X 100 ml/10 g (10%) = 960 ml Double check: 960 ml x 10 g/100 ml = 96 g Calories: 96 g x 4 kcal/g =384 kcal from protein Nitrogen content: 96 g protein x 1 gN+/6.25 g = 15.4 g Nitrogen 1 gN=6.35 g protein |
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Change the concentration
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Use 15% AA solution to “concentrate” the volume from the previous example:
Total protein needed = 96 g 96 g x 100 ml/15 g (15%) = 640 ml Volume saved: 960 ml (10%)– 640 ml (15%) = 320 ml Concentrating is generally done to conserve volume The rate will need to be adjusted to prevent excess volume from being added as more water. 80 ml/hr = 1.92L = 1920 ml – 320 ml (saved from 15% AA) = 1600 ml 1600 ml / 24 hrs = 67 ml/hr Provides same nutrients as the 80 ml/hr infusion, but less volume |
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when is the concentration of a TPN usually increased
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to conserve volume, therefore the patient receives less fluid
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compound calculations for lipids
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Lipids: 200 ml/day, 20% solution
200 ml X 20 g/100 ml (20%) = 40 g fat Calories: 200 ml/day x 2 kcal/ml (because IV, so have to look at mL)= 400 kcal from fat NOT 40 g X 9 kcal/g lipid = 450 kcal (recall composition of intralipid solutions) % of total calories from fat: 384 g CHO, 96 g protein, 40 g fat 1305.6 kcal + 384 kcal + 400 kcal = 2090 kcal 400 kcal is what % of 2090? = 19% within range because upper limit is 30% G fat/kg/day, 70 kg 40 g/70 kg = 0.57 or ~ 0.6 g/kg/day |
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Remember max % fat =
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30%
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fat max per day
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1 g/kg/day
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Potassium trending down over several days, want to increase amount provided by TPN (look at previous days requirements)
TPN @ 50 ml/hr with 20 mEq/L KCl in 1.2L |
K+ in TPN = 1.2 L x 20 mEq/L = 24 mEq K+ (baseline)
3 boluses of 20 mEq KCl given over last 24 hours 20 mEq x 3 boluses = 60 mEq K+ KPhos infusion of 20 mmol also given 20 mmol Phos x 1ml KPhos/3 mmol phos = 6.7 ml 6.7 ml x 4.4 mEq K/1 ml KPhos) = 29 mEq K+ Total K+ = 24 mEq + 60 mEq + 29 mEq = 113 mEq/K+ (only 24 from TPN) Look at why they are losing K (loop?) Incorporate a portion into TPN expressed as mEq/L have to condsider all sources K |
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sliding scale for insulin
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Same patient’s glucose has routinely been > 200 mg/dL
TPN contains 10 units/L regular insulin (1.2 L) 10 units/L x 1.2 L = 12 units Also receiving external insulin drip 4 units/hr X 8 hrs = 32 units 8 units/hr x 4 hrs = 32 units Boluses of 2 units and 4 units = 6 units Total insulin = 12 + 32 + 32 + 6 = 82 units Incorporate a portion into TPN as units/L Starting rule of thumb: 0.1 units insulin /10 gm CHO |
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Final solution of TPN
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Remember to add ~ 60 ml/1000 ml PN solution for electrolytes, vitamins/trace elements and additives
500 ml CHO + 200 ml lipid + 400 ml AA = 1100 ml 1100 ml X 60 ml/1000ml = 66 ml of additives Final volume = 1100 + 66 = 1166 ml Initiating the infusion: Protocols usually increase gradually over first several hrs to reach goal rate…examples Begin at 50% of goal rate, increase by 25 ml/hr q6 hours until goal rate reached, OR Begin at 50% of goal rate, after 12 hours increase to goal TPN will increase over the course of 12-24 hours Discontinuing the infusion: Gradually taper off over several hours: decrease rate by 25 ml/hr q1-2 hours until off or decrease rate by 50% x 2 hours, then off, for example a steroid taper If patient has only been on TPN for 3-4 days can taper over several hours |
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PN Infusion Guidelines
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Infuse admixture via pump (always)
Controls rate and volume, free-flow stop valve (safe guard so doesn’t run when stopped), alarm to detect air or circuit occlusions Continuous infusion: volume distributed continuously over 24 hours (ml/hr rate) Cyclic infusion: volume infused over 12-18 hrs Interruption to treat/prevent hepatotoxicity Helpful if multiple med administrations interrupt PN infusion Useful for home therapy patients Not ideal for glucose intolerance, diabetes, unstable fluid balance 2.4 L PN infusing at 100 ml/hr over 24 hours Same volume over 12 – 18 hours would average 200 – 133 ml/hr (this would be a good time to concentrate the TPN to decrease the rate) |
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Pharmacist’s role in TPN
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Typically order has been written when pharmacy consulted
Utilize hospital standard if it meets needs, OR Customize Should be able to assess needs from scratch and build PN or determine if a written order is appropriate or needs modified Quality assurance TPN stability, compatibility TPN labels should be clear and accurately reflect admixture components Pay attention to units: g/L, ml/day, mEq/L, mmol/L, units/L Transcription errors or misinterpretation can lead to patient harm or death (K+ mEq/L vs. mEq/day, 10.0 units insulin vs 100 units/insulin) |
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Evaluation monitoring for TPN
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Routine laboratory monitoring
Electrolytes, hematologic indices, renal function, hepatic function, functional proteins, triglycerides Need baseline values, then per protocol Other clinical measurements Weight, fluid balance (I/O), vital signs, nutritional intake (oral supplements, e.g.) Anticipate or identify complications that can be avoided or treated promptly (refeeding, compatibility) Follow trends and clinical course Not appropriate to change formula daily (inefficient, costly) PN formula at relatively fixed rate- cannot bolus to replace lytes Time from lab draw to new admixture can be 12+ hours (always a lag time) can give boluses throughout the day to make acute adjustments daily, but don’t change the TPN daily Recall time-frame for lab improvements (Alb, PAB, TFN) |
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Parenteral route for TPN
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Appropriate for short or long-term support in the absence of gut function or for suboptimal nutrition intake (7-14 days)
Venous access depends on nutrient requirements, duration of therapy and anatomy Central access (CPN/TPN) Peripheral access (PPN) PN is not emergent (adults) |
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Indications for PN
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the GI tract is still the prefered route
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Indications for PN
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Consider after 7-14 days of suboptimal nutrition intake
Assess that GI tract cannot meet needs/not tolerated: Massive small bowel resection (<50-100 cm small bowel left) Intractable vomiting when EN not tolerated (pregnancy) Severe diarrhea (malabsorption) Bowel obstruction GI fistulae (hole or corrosion connecting one part to another) Cancer Pancreatitis Cancer Critical Care (organ failure, burns) Pre-Postoperative (major GI surgery) Eating disorders (anorexia nervosa) |
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Routes of Administration for TPN
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Central or peripheral
Depends on venous access, fluid status, nutrient requirements, clinical condition, duration of needs Continue to monitor for GI function for transition to enteral or oral feeding |
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complications of TPN
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Infection, access site maintenance, compatibility, fluid balance management, phlebitis,
catheter migration or breakage, pneumothorax |
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peripherial access of TPN
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Limited to 900 mOsm/L (contact time is greater)
phlebitis, infiltration Peripheral placement in lower arms (brachial, cephalic, basilic vessel) Large volumes, diluted solutions required Easy to place unless poor veins or subjected to multiple attempts Lower risk of infection, metabolic and technical complications (<7 days) |
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central access of TPN
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Preferred > 7-14 days of hospital use or home access
Preferred to provide high nutrient requirements in patients with extensive illness or fluid fluctuations Highly concentrated Smaller volume Central veins with high blood flow will dilute hypertonic solutions enter circulation more rapidly Greater risk for infection and insertion trauma; high maintenance of access site (flushed, changed) |
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Peripheral Access sites
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Relatively easy to place at bedside in hand, mid-upper arm
Difficult if multiple attempts are made, previous vascular access, depends on quality of the vessels Short-term access (days) Limit Osmolarity to 900 mOsm/L |
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Osmolarity and TPN
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Normal serum is approximately 300 mOsm/L
Peripheral limit is 900 mOsm/L Hypertonic solutions should be given via central line to avoid phlebitis or RBC crenation due to osmotic gradient shifts |
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TPN formula, you can estimate mOsm to determine appropriate route: Dextrose, AA, lipids, electrolytes
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Dextrose = 5 mOsm/g or 50 mOsm/%
AA = 10 mOsm/g or 100 mOsm/% Lipids = 1.7 mOsm/% (essentially non-contributory/isotonic) Electrolytes = 1 – 2 mOsm/mEq |
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Central Access sites
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jugular
PICC line enters the brachial and goes to the superior vena cava throught the skin and up to the heart |
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Central Line Access
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Vary in length, lumen size and number of ports
Catheter tip terminates at superior vena cava High flow, large bore, adjacent to right heart (diluted with next HB and goes into circulation) Tip must be verified by radiography prior to use Short-term central access (weeks) Percutaneous insertion into subclavian or internal jugular vein (TLSC or IJ) Longer access (> 4 weeks) /or indefinite therapy Tunneled catheter or injection/implanted port Depends on age/anatomy, could be chemo, home TPN or antibiotics |
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Long-term central access
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Tunneled catheters
Hickman, Broviac, Groshong Subcutaneous tunnel created in chest wall to reach central vessel Secured with sutures, anchored with felt cuff to promote fibrotic tissue growth around catheter Injection port access may be external or concealed Implanted port (Portacath) Large port or reservoir surgically placed beneath skin and anchored to chest wall (accessed and de-accessed quickly) |
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PIIC line
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Intermediate use (both short and longer-term access: weeks to months) MOST COMMON
PICC = peripherally inserted central catheter Inserted peripherally (basilic, cephalic, brachial vessel) but tip advanced to the superior vena cava for central access Can handle hypertonic, large volumes Can be placed at bedside by trained personnel Acute use during hospitalization or chronic use for home care access |
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IV complications
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Insertion site infection
Catheter-related infection Phlebitis: vein irritation Thrombophlebitis Infiltration Extravasation Pain, edema, warmth, redness/streaking, oozing, blistering, fever, chills Line migration, air emboli, occlusion, breakage |
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access site care
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Site maintenance and care
Dressing changes Flush for patency SASH method Biopatch or tegaderm Antibiotic/antiseptic covering for protection; pharmaceutical-grade, sterile saran wrap Allergic reactions to tape/covering Monitor all infusions for compatibility/tolerance |
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Formulation considerations for TPN
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Available references for compatibility and stability: Trissel’s, King Guide
Exact answers not always available Conc, temp, pH, 2:1 vs 3:1, manufacturer dependent Complex admixtures containing ~ 40 items Mixing order AA, dextrose, water, electrolytes, vitamins, trace …then inspect prior to adding lipids…then inspect for uniform emulsion and phase separation Automated compounders |
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Filter recommendations for TPN
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In-line filters for PN
Recommended to reduce infusion of particulates, microprecipitates, microorganisms, pyrogens, air Multiple additives can contaminate fluid with particulates. Particles > 5 microns can cause phlebitis and obstruct flow leading to embolic complications Microprecipitates form under pH, concentration and temperature conditions (Ca-Phos) Microorganisms (most) can be removed via 0.22 µ Fat integrity is compromised when infused through this size Most appropriate for 2:1 admixtures 1.2 µ filter appropriate for 3:1 admixtures Removes particles, microprecipitates, but not most microorganisms |
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PN mixture method Two-in-one, 2:1, 2-in-1
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All micronutrients + protein (AA) + CHO macronutrients mixed in one bag
Lipids are infused separately A 0.22 μ filter is used during infusion of the 2:1 solution to reduce contamination with microorganisms, pyrogens, air Solution should be clear, inspected for particulate matter. May have yellow tinge due to AA and multivitamin/additives. |
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PN mixture method #2 Three-in-one, 3:1, 3-in-1
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All micronutrients and macronutrients (CHO, AA and lipids) are combined in one bag
Lipids create an opaque solution Alters the physiochemical properties of the mixture Unable to “see” through the mixture for obvious precipitates or particulates A 1.2μ filter is required to reduce passage of particulates and microprecipitates Instability of lipid emulsion may lead to phase separation, rendering the mixture unsafe |
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Physical appearance of TPN
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Fundamental quality assurance measure…
Just look at it! Gross particulate matter, incompatibility from gas formation, turbidity, haziness or crystallization Obvious embolic risk to the patient 2:1 admixtures should be clear-yellow (MVI, additives) 3:1 admixtures are opaque Still assess visually for emulsion destabilization Recognize the signs of phase separation Manifests as free oil droplets that layer or coalesce to varying degrees Yellow to brown in color, liberation of free oil, liquid precipitate |
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Destabilization of TPN represents
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unsafe “cracking” of the emulsion
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Stages of phase separation
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Creaming: translucent band at the surface, separate from the remaining TNA dispersion.
“light” creaming: lipid particles are destabilized, but may be resuspended upon gentle agitation of the solution. If cream layer redevelops after mixing (i.e. phase separates again), the solution should not be used “heavy” creaming: thicker/more discolored band of lipid particles Coalescence/marbling: discernable free oil droplets or layers swirled throughout the solution Cracking: Continuous liquid precipitate layer on surface |
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Lipid emulsion destabilization
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Phase separation can occur over time due to reactive cations in solution (+ charged)
The higher the valence, the greater the disruptive power: Fe3+ > Ca2+, Mg2+ > Na+, K+ Separate destabilizing cations from lipid dilution during preparation Do not hang admixture for > 24 hours When in doubt, do not infuse |
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Calcium-Phosphorus precipitation
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Calcium salts are extremely reactive and can form insoluble precipitates with several additives
Ca + bicarbonate = calcium carbonate Ca + phosphate = calcium phosphate Do not underestimate the life-threatening potential created by embolic complications |
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ways to avoid calium-phosphorus precipitation
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Use calcium gluconate as preferred Calcium donor
Use correct mixing sequence: Add phosphorus first Utilize acetate over bicarbonate for alkalinization |
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Factors increasing the risk of calcium phosphorus precipitation formation
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High concentrations of Calcium and Phosphorus salts
Use of Calcium chloride salt (more reactive) Low concentrations of AA and Dextrose Increased temperature Increased pH of admixture Improper mixing sequence Addition of IVFE and other additives |
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Role of admixture pH
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when pH is elevated = more risk for crystallization
Higher the pH (increased pH, more basic) Higher risk of crystallization Lower the pH (decreased pH, more acidic) Lower risk of crystallization |
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Metabolic complications of TPN
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Multifactorial: substrate-related, electrolyte and fluid disorders, acid-base complications
Macronutrient problems: Hyperglycemia Hypoglycemia Hypertriglyceridemia Abnormal LFT’s |
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Hepatic dysfunction and TPN
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Steatohepatitis: fatty liver infiltrates
Mild increases in LFT’s (<3 X ULN) 1-4 weeks after initiation Can reverse or resolve with formula change or d/c May be persistent in long-term home patients |
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risk factors for hepatic dysfunction and TPN
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Pre-existing liver disease, pre-existing malnutrition, sepsis, excessive calories or excessive duration of therapy, lack of enteral intake, extensive bowel surgery
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Hypertriglyceridemia and TPN
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Serum TG > 400-500 mg/dL
Main cause? IVFE-based nutrition support regimens Risk factors: liver or pancreatic dysfunction, sepsis, multi-organ failure, lipid rate and dose Defective lipid clearance Consider decreasing lipid content or holding (administer QOD, or TIW) when serum is lipemic |
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Main cause of Hypertriglyceridemia with TPN
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IVFE-based nutrition support regimens
Risk factors: liver or pancreatic dysfunction, sepsis, multi-organ failure, lipid rate and dose |
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Glucose tolerance and TPN
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Hyperglycemia
Stress, infection, steroids, pancreatitis, diabetes, excessive carbohydrate provision Reduce % or number of calories from CHO Insulin…regular only Add directly to TPN infusion Fixed dose continuous infusion Add external continuous insulin infusion Titratable infusion Hypoglycemia Abrupt withdrawal of PN, excessive insulin |
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The macronutrients
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carbohydrate, lipid and protein, are dosed on a per kg basis. These substrates are utilized to meet estimated caloric goals
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The following parameters should be calculated before recommending a nutritional support regimen:
|
Determine the weight to use for feeding. This is crucial for all calculations going forward!
Estimate the patient’s energy needs and formulate a nutrition plan using total calories to meet their energy needs. (Total calories will include carbohydrate, lipid, and protein calories). Estimate nitrogen or protein needs. Nitrogen is an atom in protein and can be dosed as grams of nitrogen or grams of protein. Ideally protein will be used to build lean body mass and not as an energy source. Determine nonprotein calories (NPC) that can be used for energy. Nonprotein calories are calories provided by carbohydrates and lipids. Determine the patient’s daily fluid needs. This will vary according to sensible and insensible losses, as well as organ function. Determine daily electrolyte, vitamin and trace element needs. Determine the most appropriate route for nutritional support: Parenteral nutrition (PN), either peripheral (PPN) or central (TPN), or enteral nutrition (EN) using the gastrointestinal tract. Enteral routes of access include nasogastric (NG), orogastric (OG), percutaneous endoscopic gastrostomy (PEG), nasojejunal (NJ), needle catheter jejunostomy (NCJ). Use the gut! |
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2. If a person is greater than ____% of their IBW, then use the adjusted body weight equation:
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120
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ABW=
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[IBW + 0.25(TBW – IBW)]
This equation means that we will fully support the patient’s lean body mass, but we will support the fat mass to a lesser degree. This is appropriate because lean body mass is more metabolically active than adipose tissue. According to the equation, we will support the adipose tissue at 25% of the rate we will support the lean body masses (or adipose tissue is 75% less metabolically active than lean body tissue). |
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If a person is less than their IBW, then use
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THEN USE TBW
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Total calories are made up of dextrose, lipids, and protein. The amount is dependent on the severity of the patient’s illness. Using our "rule of thumb" for determination of energy needs:
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Normal/Mild stress 25 kcal/kg/d
Malnourished/Moderate stress 25-30 kcal/kg/d Critically ill/hypermetabolic 30-35 kcal/kg/d Major burn/head trauma 35-40kcal/kg/day |
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values for
Protien restrinction normal/maintenance moderate stress severe stress |
Nitrogen:
0.09-0.15 g N/kg/d 0.15-0.18 g N/kg/d 0.20-0.32 g N/kg/d 0.33-0.48 g N/kg/d Protein 0.6-1 g protein/kg/d 1-1.2 g protien/kg/d 1.3-2 g protein/kg/d 2.1-3 g protein/kg/d |
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With liver or kidney dysfunction, nitrogen/protein administration may be restricted
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Increased blood ammonia levels (NH4) can lead to encephalopathy in hepatically-impaired patients. Protein restriction should be implemented during acute phases of overt encephalopathy. Increased BUN (blood urea nitrogen) can lead to uremic complications in patients with kidney impairment. However, patients receiving various forms of renal replacement therapy, or those in acute renal failure with a catabolic stressor may actually have increased protein requirements (moderate stress category
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Dosing parameters for lipid
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provide at least 2-4% of calories from lipids but do not exceed 30% of total calories
do not exceed 1 g/kg/day IV lipid |
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dosing parameters for CHO
|
do not exceed administration of 5 mg/kg/min CHO
using greater than 20-25 kcal/kg/day of CHO exceeds the mean oxidation rate of glucose |
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Complications from excess lipid administration:
|
►hypertriglyceridemia
►increased risk of pancreatitis ►immunosuppression ►altered pulmonary hemodynamics |
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Complications from excess CHO:
|
►hyperglycemi
►insulin resistance ►lipogenesis ►fatty liver infiltration |
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complications from lipid deficeincy
|
►alterations in platelet function
► hair loss ► poor wound healing ► dry, scaly skin unresponsive to water miscible creams |
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Essential fatty acid deficiency (essential fatty acids linoleic acid and alpha linoleic acid) can be avoided by providing at least ______% of the total caloric intake as lipid emulsion.
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2-4%
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1 ml of 10% propofol emulsion=
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1.1 kcal of lipids
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Monitoring Tips for lipids
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Evaluation of serum triglycerides (at least weekly) and serum blood glucose (usually Q 4-6 hours) should be a standard part of PN monitoring. Temporary interruptions of lipid infusions for 12-24 hours are recommended when the serum triglyceride level climbs over 275 mg/dL. Utilizing a 20% lipid emulsion product is preferred for PN compounding as it allows for more efficient triglyceride clearance and metabolism. If a TPN infusion is interrupted for any reason (lost access, compromised quality, electrolyte imbalance), a stock bag of 10% Dextrose (D10) should be hung and infused at the same rate as the PN formula to avoid rebound hypoglycemia.
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fluid intake for maintenance
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25-35 ml/kg/day
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abnormal fluid losses must be taken into account
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emesis, diarrhea, NG suction, fever, ventilatory circuit, wounds
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fluid intake can be estimated by
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1 ml fluid/kcal ingested
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electrolytes dependent on kidney function
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►Na, K, Mg and Phos are particularly dependent on kidney function and if renal function is reduced, intake of these electrolytes will likely need to be restricted.
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electrolytes that are sensitive to GI losses
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►Consider electrolyte adjustments through losses in the GI tract (diarrhea, emesis, fistulas), including Na, Cl, K and bicarbonate.
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diuretics may cause a loss of what electrolytes
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►Use of diuretics may cause a drug-nutrient interaction such that K, Na and Mg wasting may occur
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vitamins in TPN
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Standard adult multivitamins (10 ml) are added routinely to each daily bag of PN. They contain 12-13 known vitamins (MVI-12 does not contain vitamin K) and are based on recommended daily intake values.
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daily MVI in adult TPN
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Thiamin (B6) Riboflavin (B2)
Niacin (B3) Folic Acid Pantothenic Aid Pyridoxine (B6) Cyanocobalamin (B1) Biotin Ascorbic Acid (C) Vitamin A Vitamin D Vitamin E Vitamin K (+/-) |
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trace minerals
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Chromium
Copper Manganese Selenium Zinc Iron: not routinely added |
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why is iron not added to the TPN
|
Iron is not routinely recommended as an additive in patients receiving PN (due to stability concerns) and is not a component of current injectable trace element preparations.
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patients with hepatic problems should not receive what trace elements
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In patients with hepatobiliary disease, consider reductions of copper and manganese due to impaired excretion.
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in patients with major cutaneous problems such as burns should not receive what trace elements
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zinc, copper, selenium)
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in patients that are on TPN for extended periods of time what is the concern in regards to trace elements
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Interestingly, many components of the PN formula have been shown to be contaminated with trace elements such as zinc, copper, manganese, chromium, selenium and aluminum. In patients receiving long-term PN support, there is the concern for trace element toxicity and serum monitoring may be necessary.
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|
if the GI tracts is functional
|
it should be used for nutritional support
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are arteries or veins used for a TPN
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veins
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particles > 5 microns can cause
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phlebitis or obstucted blood flow leading to embolic complications
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|
use of a 0.22 micron filter removes
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microorganisms, but is limited to a 2-in-1 formulation without lipids
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when infusing a 3-in-1 formulation what size fliter is used
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1.2 microns
It is effective in removing both particulates and microprecipitates, however, does not remove most \microorganisms if the formulation is contaminated. |
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1 ml of 10% lipid emulsion = ___________kcal of lipid
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1.1
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1 g of lipid= _____kcal of lipid
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9
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1ml of 20% lipid emulsion = __________kcal lipid
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2
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Pay attention to nutrition admixture labels and orders! Pharmacist review and check √
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∙Formulas can be complex. Adverse events are relatively low in frequency, but can cause harm
∙Most errors associated with PN are seen with electrolytes, insulin, dextrose and additives ∙Make sure orders are clear and utilize the institution's standardized order form ∙Question large-scale changes: omissions, dramatic day-to-day fluctuations ∙Ensure compatibility of additives and appropriate administration route/filtration is used |
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Remember to add ____ml of additives for each _____ml of PN solution.
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60
1000 |
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General principles of nutrition support are the same for adults and kids
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If the gut works……..use it
Avoid over and under feeding Need a plan that outlines goals, requirements, delivery and assessment |
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if the child is older than 10 what formulas are used
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adult
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why is calcium and phosphate more problematic in peds than adults
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beceause in children their requirements are much more so more is given to them so there is more of apossibility of a percipitate
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Pediatric Nutritional Assessments pyhsical findings
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Age, weight, height, HC (head circumfrance, if the childs head is not growing than the brain is not growing), skinfold, hydration stutus
Growth is the best indicator of a child’s long-term nutritional status. Growth charts (special charts for turners and trisomy 21) Equations (rarely used) IBW= ( ht in cm 2 x 1.65 ) 1000 Growth velocity |
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Pediatric Nutritional Assessments laboratory findings
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Visceral Proteins
albumin, transferrin, retinol binding protein, prealbumin |
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what is better EN or PN
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Enteral Nutrition: Superior to Parenteral
Trophic effects on intestinal villus Reduces bacterial translocation (if the gut is not used membranes become leaky and it is easier for bacteria to pass through) Supports Gut-associated Lymphoid Tissue Promotes secretory IgA secretion and function Lower cost |
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PN nutritional problems
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IV access
Infectious risks PN-associated liver disease |
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Enteral Feeding in Pediatrics
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Healthy term infants: breast or bottle fed
Preterm infants (even healthy), sick term infants and critically ill children : NG-tube, OG-tube, G-tube Premature infants are known to suck but 'forget' to breathe and swallow need feeding tube Generally begin with continuous “tropic feeds” with slow transition to bolus feeds and ultimately oral feeds |
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when to initiate EN in peds
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ASAP
they have to be hempdynamically stable |
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do you start with bolus feedings or continuous feedings in peds
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continuous because it is easier for the body to except the smaller feedings
work up to bolus |
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Does Breast Milk Provide Complete Nutrition?
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The American Academy of Pediatrics (AAP) recommends human milk as the preferred feeding for all infants
Pre-term breast milk is insufficient in calories, protein and minerals need BM supplements/fortifiers Enteral nutrition can be provided to premature infants with commercial premature formulas. |
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what is supplemented to breast milk in preterm infants
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higher concentrations of protein, Ca, phos
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Premature Infant formulas
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Higher caloric density
Higher Ca, P and protein |
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Standard Infant formulas
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Cow Protein Based: Enfamil Lipil, Similac Advance
Soy Protein Based: Isomil Advance Other Cow Protein Based: Enfamil Lactofree Lipil, Similac Lactose Free Advance |
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Overview of Formula Choices
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Formula throughout the years: premature infant, infant less than 1 yr old, specialized, pediatric (1-10 yrs old) and adolescent/adult (greater than 10 yrs old)
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how long is considered full term
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45 weeks
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Specialty Infant Formulas
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Hydrolyzed Protein: “broken down” protein – great for malabsortion syndromes
Amino Acid based: great for severe food allergies Portagen: 87% MCT (median chain TG) fat. Indicated for long chain fat intolerance Ross Carbohydrate Free: for carbohydrate intolerance Similac 60/40: for renal disease 3232 A: for irretraceable diarrhea Transitional Infant Formula: follow-up formula for ex-preemies. Higher protein, Ca and P content than standard formula. |
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Pediatric Formulas (Ages 1-10) oral
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Pediasure: (choc, van, straw, banana cream and orange cream) standard complete pediatric oral supplement. 240 calories per can.
Carnation Instant Breakfast: (choc, van, straw) powder, mix with milk, affordable substitute for Pediasure. Boost: (choc, van, straw) standard adult and pediatric oral supplement. 240 calorie per can. Boost Breeze: (tropical, mixed berry) juice oral supplement, not complete. 180 calories per can. Health Shake: (choc,van,straw) milk based, 300 calorie per 6 ounces supplement. Comes frozen. not all are complete feeding formulas |
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Pediatric Formulas (Ages 1-10) tube feedings
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Tube Feeding (eg Kids in the ICU)
Nutren Jr. with and without fiber Peptamen Jr.: semi-elemental (broken down) and 60% MCT fat, no fiber. Ready to feed can. 250 calorie per can. Specialty (tube) Vivonex Pedatric: Malabsorption and fat intolerance, Pancreatitis. |
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drawbacks to EN
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Gastric emptying impairments such as vomitting which can lead to aspiration
Aspiration of gastric contents Diarrhea Sinusitis from NG tubes Esophagitis /erosions Displacement of feeding tube |
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Contraindications to Enteral Feedings for peds
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Nonfunctional gut, anatomic disruption, gut ischemia
Massive small bowel resection (SBS) Necrotizing enterocolitis (NEC) Severe peritonitis Severe IBD Intractable diarrhea Gut GVH (graft vs. host disease) Severe shock and MODS (liver, renal, pulmonary, pancrease) these patients are hemodynamically unstable the above patients would require TPN |
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JP is a premature infant (born at 26 weeks) who is now day-of-life 7. He remains on mecanical ventilation (orally inserted ETT) and his nutrition (until today) has been supported solely by TPN, but now, he is ready to start enteral feedings.
1) What would be the best route of enteral feeding for JP? a) PO bolus b) NG bolusc) NG continuous d) OG continuous 2) Which formula is best suited for JP? a) boost b) enfamil-24 c)vivonex d) pulmocare |
c) NG continuous
b) enfamil-24 |
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Indications for PN in Pediatrics
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When EN is unlikely to provide adequate nutrition
Prematurity (ASAP) Limited reserve with high metabolic demand Immature GIT Critical period of brain growth Other Infants and Kids within 3-7 days Functional or Anatomical Problems with GIT GI anomalies, severe inflammatory disease, persistent diarrhea/vomiting trauma, solid organ failure, anorexia, CF, CHI, spinal cord injury, post-surgical, CHD, cancer |
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Routes of PN Administration in Pediatrics
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Peripheral (PIV)
* Short-term use only Central * Broviac, Hickman * Port (for ambulatory patients with long term PN) * Umbilical vessels (3 vessels: 2 arteries, 1 vein) good for 10-14 day use |
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All of the following are appropriate candidates for parenteral nutrition EXCEPT:
a) premature infant (27 weeks gestation) who is 1 day old b) seven year old who refuses to eat solid food and has lost 5 pounds c) ten year old in the PICU with GI trauma d) two year old who is 1 day s/p liver transplant |
b) seven year old who refuses to eat solid food and has lost 5 pounds
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When to Initiate PN in Children?
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Preemie: within hours of birth
Infant: within 1-3 days of substandard nutrition Child: within 5 days of substandard nutrition Adolescent: within 7 days of substandard nutrition Adult: 7 days The younger the patient the faster the PN initiation Initiation is age dependent |
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Fluid Requirements in peds
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Insensible Losses
perspiration or evaporative via skin Can be huge in micropreemie ( < 750 grams) * lack of stratum cornium so there is a large amount of water loss respiratory tract Reduced when mechanically ventilated (lower fluid requirements because are not breathing of water) Sensible Losses Urine Stool Wounds Drains (chest tube, JP drains etc) |
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how are fluids administered to peds
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all in the TPN
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neonate fluid requirements
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Neonate: 110 -150 ml/kg/day
200 ml/kg/day in the micropremie 80 ml/kg/day in severely fluid restricted term infant Fluid in the neonate is advanced as the infant transitions from acutely ill to “feeding and growing” |
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child fluid requirements
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Child
1-10 kg: 100 ml/kg/day 10 -20 kg: 1000 ml + 50 ml/kg for each kg over 10 above 20 kg: 1500 ml + 20 ml/kg for each kg over 20 |
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what happens to fluid requirements as age increases
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it decrease on a ml/kg basis
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Total energy expenditure (TEE) =
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REE + energy for activity + energy for growth
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The younger you are….the ______ your total caloric requirement will be (kcal/kg/day)
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higher
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Energy or Calorie Requirements
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Neonate: 100-120 - Infant (0.5-1 yr): 90-110
Child (1-6): 70-80 - Adolescent (7-10): 55-65 11-14 yrs: 40-50 - 15-18 yrs: 30-40 Predictive Equations and Nomograms BMR= 22.1 + (31.03 x wt in kg) + 1.16 x length in cm) Harris Benedict (kids > 15 yrs) male: 13.75 (W) + 5(H)- 6.76(A) +66.47 female: 9.56(W) + 1.85 (H) - 4.68 (A) + 655.1 |
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what does more stress on the body to caloric demands
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increases caloric energy expenditure so increases demands
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in the hospital the REE increases and what happens to energy for activity and energy for growth
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they do not increase
as a result: kids will have reduced total energy requirements during acute illness |
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TEE is NOT increased in critically ill neonates and children with early illness
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When it comes to stress and EE…. Children are not small adults
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Late illness with Lower Stress =
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Elevation in TEE
increased energy expenditure …..as kids get better, they have higher energy needs Avoid overfeeding during acute illness! |
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Early Illness with High Stress does not equal
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Elevation in TEE
Energy equations are NOT accurate in the ICU…must measure! |
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Early acute stress, due to trauma or surgery, can have the following physiologic effects and outcomes on a child:
a) activation of neuroendocrine and cytokine response b)increase in heart rate, minute ventilation and tissue oxygen demand c) increased total energy expenditure d) all of the above e) a and b only |
e) a and b only
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Carbohydrate (Dextrose) in peds
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Initial dose is based on previous glucose tolerance
Generally start with 5-10 % dextrose and advance by 2.5-5% as tolerated. The price of exceeding the maximum glucose oxidative capacity and excessive glucose metabolically expensive pathways such as glycogen storage and lipid synthesis will be favored increased energy expenditure, increased carbon dioxide production fatty infiltration of the liver |
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do you start peds at goal range with dextrose
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no start with D5 or D10 and determine if they are tolerating it and if they are can increase by 2.5-5%
in smaller children advance more slowly |
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hyperglycemia and peds
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Glucose enters the cells of GIT, neurons, heart, liver etc, via the aid of glucose transporters.
This process (except in skeletal muscle) is INDEPENDENT of insulin – so the higher the serum glucose the higher the intracelluar transport of glucose into the cellular mitochondria. As glucose enters the Krebs cycle for ATP production free radicals (O-) are produced morbidity and mortality. |
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what level do you want serum glucose at in peds
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< 180
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Specialized Pediatric Protein
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Trophamine, Aminosyn PF, Premasol (plus cysteine)
Generally initiated at GOAL (in infants and children) Preemie: 3-4 grams/kg/day Short titration in preemie (initiate at 2 g/kg) Infant-1 year: 2-2.5 grams/kg/day 1-6 years: 1.5-2 grams/kg/day 6-14: 1-2 grams/kg/day 15-18 years: 1-1.5 gram/kg/day Hesitation to provide protein will exacerbate the semi-starvation state of the preemie in the first week(s) of life |
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do you start at goal with TPN proteins for peds
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yes, except in micor-preemies give them 1/2 of the goal value because of tolerance
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what 2 enzymens are peds missing
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hepatic cysteinesulfinic acid decarboxylase
hepatic cysathionase |
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what to aa are peds deficient in
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cysteine
taurine |
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conditionally essential aa in peds
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cysteine
taurine glutamine carnitine arginine |
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glutamine in peds
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preferred fuel for the gut, maintains gut integrity, important during stress
supplementation can reduce PN duration IV stability issues |
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carnitine in peds
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required for transport of FFA into mitochondria for ß-oxidation and energy production; clinically appears as intolerance of IVFE
newborns are at risk of deficiency secondary to immature synthesis and lack of AA in PN |
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arginine in peds
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precursor for nitric oxide, improves wound healing
especially for burn victums |
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Fat (Intravenous Lipid Emulsion) peds
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Integral part of cell membranes, platelet function, hormones, inflammatory mediators, wound healing and brain development
Concentrated source of calories Commercially available IVFE differ in percent (10-30%) and source of TG (soybean or combination of soybean and safflower) Contains egg phospholipids and glycerol |
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if a ped has a egg allergy can they receive the lipid emulsion
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no
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Absolute minimum requirement of fat for peds
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1-4% of total calories (prevents essential FA deficiency)
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Typical intake of fat for peds
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1-3 g/kg/day (30% of calories in older child and 40-60% in neonates and young infant)
Intake is limited by ability to clear TG and FFA dependent of lipoprotein lipase, hepatic lipase and lecithin cholesterol acyltransferase |
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when should IVFE started in peds
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IVFE should be started on the first day of therapy at 0.5-1 g/kg/day and advanced daily by 0.5-1g/kg/day as tolerated
Generally infused over 20-24 hours |
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goal serum TG in peds
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Follow serum TG (goal < 150-200 mg/dl)
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IVFE and Toxicity in peds
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Fat accumulates inside phagocytes impair immune function (overwhelms the phagocytes)
Fat alters pulmonary vascular tone by shifting the AA pathway towards thromboxane (causes vasoconstriction) and away from prostaglandin leading to increased PVR FFA can displace bilirubin from albumin All toxicity is dose and infusion-rate related! Infuse lipid over 20-24 hours Avoid > 0.5 g/k/day in infants with elevated TB Check serum TG during septic events IVFE can cause hydroperoxide production when exposed to light….cell damage…….protect from light!! |
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infuse lipids over _____________ hours
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20-24 hours
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all toxicities in regards to lipids and peds is due to....
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infusion rates
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The presence of what allergy makes intralipid contraindicated?
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egg
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The use of which sedative can provide a potentially significant amount of calories (as fat) and may require an adjustment in the nutritional regimen?
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propofol
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Is there a better fat out there for peds?
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Current IVFE are composed of omega-3 and omega-6 polyunsaturated long-chain triglycerides
Medium-chain triglycerides are gaining interest MCT are cleared faster Do not accumulate in the liver Do not require carnitine But..are not a source of essential FA Mix of MCT-LCT are being investigated and are in use in Europe |
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When starting parenteral nutrition in a child, which of the following statements is TRUE?
a) amino acids (protein) should be started at GOAL b) fat emulsion (lipid) should be started at GOAL c) glucose (dextrose) should be started at GOAL |
a) amino acids (protein) should be started at GOAL
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Vitamins for peds
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Vitamin stores cross the placenta during the last trimester
There is NOT a MVI product designed specifically for premature infants with higher A and lower B vitamins Dose: 2 ml/kg up to 5 ml Peroxides are generated by MVI when exposed to light AND Vitamin A is lost when exposed to light…..Protect from light! peds do not have their own vitamins |
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Trace Elements
in peds |
Zn, Cu, Mn, Cr, Se
with renal disease reduce Se (unless they are on RRT); with high ostomy output increase Zn with cholestatic disease, give 1/2 of Cu and zero Mn they don't need all of them right away, but they give them anyways once the child >11 use the adult formulation |
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26 week preemie on DOL 1 transferred from outside hospital. Wt= 600 grams. Ventilated, on antibiotics.
Fluid rate = 3.5 ml/hr, patient has a UVC and UAC Current IVF = D7.5% + 1 unit heparin/ml at 3 ml/hr Electrolytes are WNL, Glucose= 100 How would you initiate IV dextrose Protein Fat |
dextrose: tolerating D7 so could increase to 7.5-10
protein: 2-4 mg/kg/day fat: goal is 3 mg/kg/day, but start with 0.5-1 mg/kg/day on use TG to see if tolerating |
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10 year old, s/p MVA with BAT, femur fractures and ventilated. Is post-trauma day #4 and team wants to start TPN.
Weight = 32 kg (50th percentile) Currently NPO, on D51/2NS + 20 mEq KCl/L Labs: 140/103/8 glucose= 250 Ca: 4.2 Alb: 1.9 3/ 25/ 0.4 P: 4 Mg: 1.2 Identify abnormal labs How would you initiate and advance TPN? |
Glucose is high
Ca is low D5 + insulin protein: 1.5-2 mg/kg/day (starting at goal) fat: 1 mg/kg/day |
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What would be the initial TPN composition for a 25 kg 5 year old child with a central line, currently tolerating 5% dextrose
Glucose 10%, Protein 2 g/kg/day, lipids 5 g/kg/d Glucose 10%, Protein 1 g/kg/day, lipids 15 g/kg/d Glucose 15%, Protein 0.5 g/kg/day, lipids 3 g/kg/d Glucose 12.5%, Protein 0.2 g/kg/day, lipids 1 g/kg/d Glucose 10%, Protein 2 g/kg/day, lipids 1 g/kg/d |
Glucose 10%, Protein 2 g/kg/day, lipids 1 g/kg/d
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Electrolytes Requirements child vs. adult
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Children
Na = 2 - 4 mEq/kg/day K = 2 - 4 mEq/kg/day Cl: Acetate = 1:1 Mg = 0.3 - 0.5 mEq/kg/day P = 0.5 - 2 mEq/kg/day Ca = 0.5 - 3.5 mEq/kg/day (a lot more CA and Phos because of bone growth) Adults Na = 1 -2 mEq/kg/day K = 1 - 2mEq/kg/day Cl: Acetate = 1:1 Mg = 8-20 mEq/day P = 20 - 40 mmol/day Ca = 10-15 mEq/day |
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hyponatremia in peds
|
Na+ less than 130 mEq/L
Severe: less than 120 mEq/L Mortality as high as 50% |
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causes of hyponatremia in peds
|
SIADH
Too much free water Large losses (diuretics/CSW) |
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Symptomatic Hyponatremia in peds
|
Cerebral Edema
Nausea, vomiting Decreased LOC Coma Seizures Respiratory arrest Death |
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Non-osmotic stimulators of AVP (anti-pee/ADH)
|
Hypotension, hypovolemia
CHF Cirrhosis Nephrotic syndrome Nausea, vomiting Pulmonary disease, mechanical ventilation CNS disturbances: meningitis, encephalitis, tumors, injury Hypoglycemia Hypoxia, hypercarbia Stress, fear, pain Postoperative state |
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Recommendations in peds to prevent hyponatremia
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Do NOT use hypotonic IVF for hospitalized children
Plain dextrose 5% ½ NS or ¼ NS D5 1/4NS (without K+) DO use 5% Dextrose 0.9% NaCl 0.9% NaCl Does not apply to Premies and neonates High risk for fluid overload Ongoing free water losses |
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2 y.o. girl, severe status asthmaticus, hypercarbic respiratory failure requiring intubation
Sedation, neuromuscular blockade, dynamic hyperinflation on mechanical ventilation Arterial PCO2 remains around 120 (very high) D5 1/4NS at maintenance Urine output 3-4 mL/kg/hr 18 hours later: Na+ decreased from 138 to 128mEq/L Pupils fixed and dilated Which factors put the patient at risk for cerebral edema? |
hyponatremia
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Steps to Take When Working with Electrolyte Replacements in peds
|
ALWAYS confirm the patient’s laboratory values
Electrolyte replacement must be given in a slow, deliberate manner Ca: over 30 min K: over 1 hour P: over 4-6 hours Mg: over 2 hours Careful with compatibility issues Know what kind of access your patient has the type of line is important because will use different concentrations |
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Monitoring in Children
|
Daily weight
Weekly HC and length in infants Serum chemistry Daily while acutely ill and increasing intake Weekly thereafter Chem-7 with Ca, P, Mg Protein Panel Do not over-monitor serum- phlebotomy loss leads to anemia |
