Dextrans

Uses

Dextran 70, so-called because its molecules have an average weight of 70 kDa, is used as a plasma substitute, as is dextran 40. Dextran 40 has been used to improve blood flow in ischemic limbs. Dextran 40 and dextran 70 have been used to prevent deep venous thrombosis. Dextran 1 is used as a desensitizer to prevent allergic reactions to dextrans of larger molecular weight. After reproductive surgery 32% dextran 70 is sometimes administered intraperitoneally in an attempt to reduce the formation of adhesions.

Dextran deposition in tissues

In biopsy and autopsy studies 32 patients treated with regular hemodialysis for an average of 61 months, who had also received dextran 40 as a plasma expander because of hypotension during hemodialysis, were compared with a control group of 11 hemodialysed patients who were given other plasma expanders. In 11 of the former who had received the largest dose of dextran 40 (0.38 g/kg/week), particles were found in the cytoplasm of macrophages in various organs, which were PAS-positive and diastase resistant on light microscopy and birefringent on polarization. Electron microscopy showed a fibrillar structure, but ionic analysis by electronic sampler on scanning electron microscopy excluded silicone. No intracellular inclusions were observed in the control group, or in the patients given dextran 40 in doses lower than 0.08 g/kg/week. There was a linear relation between the number of particles and dose of dextran 40 that had been given, leading the authors to suggest that the material demonstrated in the macrophages was dextran that had been structurally modified and conglomerated by macrophage activity to a water-insoluble form [ ].

Cardiovascular

High output left ventricular failure has been described after hysteroscopic lysis of adhesions using dextran as a distension medium. Prolonged surgical dissection of the uterine wall (the precise duration of the operation was not stated in the report) and the large volume of dextran and fluid (2 liters of 5% dextrose and an additional 800 ml of dextran) probably caused the dextran to enter into the systemic circulation, inducing a significant shift of fluid into the intravascular compartment [ ].

Respiratory

Pulmonary edema and coagulopathy following intrauterine instillation of 700 ml of 32% dextran 70 has been reported [ ]. The volume exceeded that recommended by the manufacturer (500 ml), and the installation time (2 hours) was in excess of that recommended (45 minutes). The authors pointed out that hyperosmolarity of the agent is such that if it enters the intravascular compartment, volume overload can result, since 100 ml of intravascular dextran 70 will osmotically expand the intravascular volume by 860 ml, by drawing interstitial fluid into the central compartment. This can further aggravate the risks of pulmonary edema and dilutional coagulopathy.

Dextrans can also cause non-cardiogenic pulmonary edema and/or respiratory distress syndrome.

• Adult respiratory distress syndrome occurred after the intravenous infusion of dextran 40 in a 30-year-old woman, a smoker with a history of insulin-dependent diabetes mellitus, who had sustained an acute inferior myocardial infarction; the dextran was given in preparation for possible stent placement after angioplasty of the right coronary artery [ ].

• A 43-year-old woman underwent delayed breast reconstruction 9 months after modified radical mastectomy and received 4 liters of crystalloid intraoperatively [ ]. Postoperatively she was given an infusion of dextran 40 preceded by a small dose of dextran 1. On the next 2 days she was febrile, with no respiratory symptoms, although her oxygen saturation was 83%. On the third day, she was febrile and dyspneic, with a respiratory rate of 29 breaths per minute. Her oxygen saturation fell to 70%. A chest X-ray showed diffuse alveolar infiltration. Dextran was withdrawn. Her lungs worsened, and on day 6 she required intubation for worsening hypoxia, dyspnea, and tachypnea. A chest X-ray showed bilateral alveolar consolidation and other signs consistent with respiratory distress syndrome. Her oxygenation slowly improved and extubation was possible on day 11.

• Acute pulmonary edema developed in a healthy patient after elective microsurgery for treatment of a malignant tumor of the forearm [ ]. The patient was in good physical condition before the operation, and there was no sign of volume overload perioperatively. Cardiac enzymes, electrocardiogram, and echocardiogram were normal. No other medications were likely to have caused the pulmonary edema. The gradual response to diuretics suggested a non-cardiogenic cause.

Although thromboprophylaxis of microvascular anastomoses seems advisable theoretically, there is little clinical evidence to support the use of dextran for this purpose. The pulmonary edema in these cases was thought to be non-cardiogenic, similar to that caused by heroin, methadone, propoxyphene, and salicylates, due to a direct adverse effect on the pulmonary vasculature, rather than anaphylaxis, cardiac pump failure, or volume overload.

Severe pulmonary edema developed in a patient who underwent breast reconstruction in whom dextran was used to improve the deterioration of flap perfusion during the postoperative period [ ].

• A 48-year-old white woman underwent right modified radical mastectomy for infiltrative ductal carcinoma. She was given dextran 40, 10 ml/kg, on the second postoperative day because of partial ischemic changes in the flap. She then had nausea, vomiting, and fever, and 10 hours later developed dyspnea and chest pain, which worsened on the following day. Chest radiography showed bilateral pleural effusions and bilateral reticulonodular opacities that were interpreted as pneumonic infiltration. She did not have hemoptysis or pleuritic chest pain, and there were no signs of heart failure. She had a leukocytosis (16.4 × 10 ⁹ /l). Cultures of sputum and fluid aspirate were negative. On postoperative day 4, her dyspnea worsened, her PO ₂ fell, and her pH rose to 7.53. Lymphangitic carcinomatosis was considered, but this was not supported by cytology of the effusion fluid or tumor markers. Her history of allergic reactions suggested the possibility of dextran-induced severe pulmonary edema leading to respiratory distress syndrome. Dextran was withdrawn and she was given an intravenous bolus dose of prednisolone 250 mg. Her symptoms rapidly improved and she recovered gradually over the following week.

Although severe pulmonary edema with respiratory failure is not a typical allergic reaction to dextrans, this case illustrates that it cannot be discounted.