Clay-Induced Permeability Damage from Injected Scale Inhibitor Solutions

We conducted an experimental investigation of the formation damage caused by the interaction of common scale inhibitor chemistries with reservoir clays. It is important to minimize permeability loss during scale inhibitor squeeze treatments because this process involves injecting a high concentration inhibitor solution into the near wellbore region of a producer. One motivation for this study was to explain the formation damage observed after some squeeze treatments in a California field.

Two types of sandstones were studied: unfired Berea (100-200 md, has nonswelling, kaolinite clay) and a San Joaquin Valley reservoir rock (1-10 md, has swelling, smectite clays). We performed a series of corefloods to examine the tendency of these scale inhibitor solutions to reduce permeability via clay deflocculation, swelling, or dispersion over a wide range of NaCl salinities.

Two scale inhibitors were tested: diethylenetriaminepenta (methylene phosphonic acid) (DETPMP) and a phosphino-polycarboxylic acid (PPCA). Neutral pH solutions were used in all coreflood experiments to prevent mineral dissolution and other complicating effects. Some floods included a preflush with a clay stabilizer (dimethylamine-epichlorohydrin copolymer — DEC). The experimental program included X-ray diffraction (XRD) studies to verify inhibitor/clay damage mechanisms indicated by the coreflood results.

Results and Conclusions are:

1. The minimum salinity required to prevent damage (critical salt concentration — CSC) is roughly twice as high in the California sandstone versus Berea sandstone, with or without inhibitor present (Figure 1 and 2).

2. At any given sodium salinity, brines containing either type of scale inhibitor caused more damage to both sandstones than NaCl brines (no scale inhibitor). See Figures 1 and 2.

3. Clay-related permeability loss can be avoided by using a makeup brine with a salinity that is greater than the CSC for that scale inhibitor solution/rock combination.

4. In Berea sandstone, a DEC clay stabilizer preflush eliminated formation damage caused by injection of DETPMP (even in distilled makeup water). However, severe damage occurred in Berea cores where the DEC preflush was followed by the PPCA, due to an incompatibility between DEC and PPCA.

5. For the California sandstone, a DEC preflush reduced, but did not eliminate formation damage for both inhibitor types (Figure 3). In this case there was no apparent DEC/PPCA incompatibility. XRD studies indicate that the stabilizer was adsorbed into the interlayers of the smectite structure, thereby reducing the interaction with the inhibitor.

6. Formation damage associated with scale inhibitor squeezes in this California field were the result of in-situ emulsions, not clay swelling or migration.