Section 3 - Complications of TPN

Introduction

Mechanical, metabolic, and septic complications are associated with PN therapy. Mechanical and septic complications are related to obtaining and maintaining a route of central vascular access. Metabolic complications require both a thorough assessment of patients prior to initiation of PN and close monitoring while receiving PN. Careful attention to detail minimizes complications.

Mechanical complications

Mechanical complications are primarily related to the initial placement of a central venous catheter. Improper placement may cause pneumothorax, vascular injury with hemothorax, brachial plexus injury or cardiac arrhythmia.

Venous thrombosis is one of the two most common problems that occur after central venous access is established. The other is infection. Venous thrombosis is associated with significant morbidity rates. Signs include distended neck veins and swelling of the face and ipsilateral arm. The risk of venous thrombosis is greater if patients are dehydrated, have certain malignancies, have had prolonged bed rest, have venous stasis, have sepsis, or have hypercoagulation. Additional risk factors include morbid obesity, smoking, or ongoing estrogen therapy.

Infectious complications

PN imposes a chronic breech in the body's barrier system. The infusion apparatus from container to catheter tip may prove a source for the introduction of bacterial or fungal organisms. The operator inserting the venous catheter, the pharmacist compounding the solution, or the care-giver hanging the bag or changing the site dressing may contaminate the patient's "lifeline."

Infection is one of the two most common problems that arise after central venous access is established. The other is venous thrombosis, discussed earlier. The mortality rate from catheter sepsis may be as high as 15%.

The primary preventive measures include adhering to strict aseptic procedure while establishing access and providing care of the dressing and line, and prohibiting the use of the TPN line for other purposes. Other preventive measures include:

• Changing the dressing routinely (every 48-72 hours) or when it becomes soiled, wet or loose. The care-giver should wear a mask and gloves while changing the dressing.
• Extending the application of antimicrobial solution at least 1 inch beyond the final dressing.
• Placing a sterile sponge over the catheter, then placing an occlusive dressing.
• Inspecting the site for tenderness, erythema, edema, loose sutures, or drainage.
• Changing the TPN intravenous tubing every 48 hours. A 0.22-µm in-line filter should be used whenever fat is not being infused.
• Avoiding violation of TPN catheters for central venous pressure monitoring or the administration of intravenous medications or blood products.

Metabolic complications

Metabolic complications fall into two broad categories: early and late complications. Those in the first category occur early in the process of feeding and may be anticipated. They are avoided by careful monitoring and appropriate adjustment of intake. Late metabolic complications are less predictable. They may be caused by an exacerbation of preexisting abnormalities, unpredictable long-term requirements, inadequate solution composition, or failure to monitor adequately.

Metabolic complications of PN

Early complications	Late complications
Volume overload	Essential fatty acid deficiency
Hyerglycemia	Trace mineral deficiency
Refeeding syndrome	Vitamin deficiency
Hypokalemia	Metabolic bone disease
Hypophosphatemia	Hepatic steatosis
Hypomagnesemia	Hepatic cholestasis
Hyperchloremic acidosis

Fluid and electrolyte complications

Electrolyte management is one of the most difficult aspects of PN therapy. Often electrolytes are outside of the normal range based on an underlying cause rather than directly related to the PN solution. For this reason, no specific guidance can be given to adjust individual electrolytes based on laboratory serum concentration. Instead, incremental dose adjustments are made concurrent with treatment of the underlying cause of electrolyte abnormality. Patient acuity will prescribe the magnitude of dosing adjustments as well as the need for more frequent monitoring. In general, supplemental electrolyte doses in response to an acute underlying condition are best managed outside of PN therapy.

Sodium - Normal = 135 - 145 mEq/L

	Excess (Hypernatremia)	Deficiency (Hyponatremia)
Contributing Factors	Dehydration Diabetes Insipidus Excess sodium intake	Excess Fluid Hyperlipidemia Hyperproteinemia Hyperglycemia Gastrointestinal, Skin and Renal Losses SIADH (Syndrome of Inappropriate Antidiuretic Hormone)
Signs & symptoms	Thirst Restlessness Irritability Tremulousness Spasticity Hyperreflexia Ataxia Seizures Coma Intracranial Bleeding	Bloating Headache Anorexia Muscle cramps Nausea Vomiting Lethargy Seizures Cerebral edema Increased Intracranial Pressure
Intervention	Replace fluid deficit Check for excess sodium intake Check blood sugar	Decrease fluid intake Check for causes of fluid retention Check for causes of sodium loss Administer sodium if patient at risk for seizures

Potassium - Normal = 3.5 - 5.0 mEq/L

	Excess (Hyperkalemia)	Deficiency (Hypokalemia)
Contributing Factors	Acidosis Insulin Deficiency Chemotherapy Rhabdomyolysis Burns Renal Dysfunction Excessive Potassium Intake Potassium Containing Drugs	Vomiting Diarrhea Draining Fistulas Diuretic-Induced Renal Losses Metabolic Alkalosis Plasma Volume Contraction
Signs & Symptoms	Muscle Weakness Arrhythmias	Myalgias Weakness Cramps Bradyarrhythmias Heart Block Paroxysmal Atrial Tachycardia Paralytic Ileus
Intervention	Restrict potassium intake Identify and correct underlying cause	Replace potassium deficit Check for magnesium deficiency Identify cause of potassium loss Check for re-feeding syndrome

Magnesium - Normal = 1.5 - 2.0 mEq/L

	Excess (Hypermagnesemia)	Deficiency (Hypomagnesemia)
Contributing Factors	Renal dysfunction Excessive intake	Gastrointestinal malabsorption Renal wasting disorders (drugs, alcoholism) Insufficient intake Parathyroid disease
Signs & Symptoms	Hyporeflexia Muscle weakness Flaccid paralysis with respiratory depression Lethargy Sedation Stupor Coma Hypotension Sinus bradycardia	Neuromuscular hyperactivity Tremor Twitching Hyperreflexia Paresthesias Tetany Seizures Apathy Depression Agitation Ventricular fibrillation and tachycardia
Intervention	Check renal function Check for sources of excess intake	Check for re-feeding syndrome Identify cause of excess losses Replace magnesium deficiency

Calcium - Normal = 8.5 - 10.5 mg/dl

	Excess (Hypercalcemia)	Deficiency (Hypocalcemia)
Contributing Factors	Neoplasia with bone metastases Hyperparathyroidism Drugs (thiazides, lithium, vitamin A & D, calcium supplements) Immobilization Carcoidosis Tuberculosis Beryliosis	Hypoalbuminemia Hypoparathyroidism Metabolic and respiratory alkalosis Vitamin D Deficiency Drugs (furosemide, calcitonin, phenytoin, barbiturates, mithramycin, oral phosphorus)
Signs & Symptoms	Anorexia Nausea Vomiting Constipation Polyuria Polydipsia Renal failure Nephrolithiasis Metastatic calcification	Tetany Paresthesias Muscle spasms and cramps Carpopedal spasms Fatigue Irritability Depression Confusion Delusion Seizures Decreased myocardial contractility
Intervention	Reduce calcium intake Identify and treat underlying cause Consider overdose of Vitamins A or D as a cause Consider hydrating the patient	Evaluate the accuracy of the lab results based on albumin levels Replace calcium deficit Replace protein deficit Replace Vitamin D deficit Remove excess phosphate intake Identify and treat underlying cause

Phosphorus - Normal = 3.0 - 4.5 mg/dl

	Excess (Hyperphosphatemia)	Deficiency (Hypophosphatemia)
Contributing Factors	Renal dysfunction Hypoparathyroidism Excessive intake Rhabdomyosis Chemotherapy	Phosphate binding drugs (sucralfate, aluminum/magnesium containing antacids, calcium carbonate) Burn recovery Respiratory alkalosis Diabetic ketoacidosis Alcoholism
Signs & Symptoms	Symptomatic hypocalcemia Calcium phosphate deposition in bone and soft tissue	Irritability Apprehension Wakefulness Confusion Acute respiratory failure Decreased cardiac contractility Hepatocellular dysfunction Anorexia Nausea Hemolysis Red blood cell or platelet dysfunction
Intervention	Reduce phosphate intake Identify and treat underlying cause Consider the use of phosphate binding drugs	Check for re-feeding syndrome Replace phosphate deficit slowly to avoid hypocalcemic tetany Identify and treat underlying cause

Refeeding syndrome

Refeeding of severely malnourished patients may result in "refeeding syndrome" in which there are acute decreases in circulating levels of potassium, magnesium, and phosphate. The sequelae of refeeding syndrome adversely affect nearly every organ system and include cardiac dysrhythmias, heart failure, acute respiratory failure, coma, paralysis, nephropathy, and liver dysfunction.

The primary cause of the metabolic response to refeeding is the shift from stored body fat to carbohydrate as the primary fuel source. Serum insulin levels rise, causing intracellular movement of electrolytes for use in metabolism.

The best advice when initiating nutritional support is to "start low and go slow". Recommendations to reduce the risk of refeeding syndrome include:

• Recognize patients at risk
  • Anorexia nervosa
  • Classic kwashiorkor or marasmus
  • Chronic malnutrition
  • Chronic alcoholism
  • Prolonged fasting
  • Prolonged IV hydration
  • Significant stress and depletion
• Correct electrolyte abnormalities before starting nutritional support
• Administer volume and energy slowly
• Monitor pulse, I/O, electrolytes closely
• Provide appropriate vitamin supplementation
• Avoid overfeeding

Section 3 - Complications of TPN

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